Blood pressure(BP) is thepressureofcirculating bloodagainst the walls ofblood vessels.Most of this pressure results from theheartpumping blood through thecirculatory system.When used without qualification, the term "blood pressure" refers to the pressure in abrachial artery,where it is most commonly measured. Blood pressure is usually expressed in terms of thesystolic pressure(maximum pressure during oneheartbeat) overdiastolic pressure(minimum pressure between two heartbeats) in thecardiac cycle.It is measured inmillimeters of mercury (mmHg)above the surroundingatmospheric pressure,or inkilopascals(kPa). The difference between the systolic and diastolic pressures is known aspulse pressure,[1]while the average pressure during a cardiac cycle is known asmean arterial pressure.[2]

Blood pressure
A healthcare worker measuring blood pressure using asphygmomanometer.
MeSHD001795
MedlinePlus007490
LOINC35094-2

Blood pressure is one of thevital signs—together withrespiratory rate,heart rate,oxygen saturation,andbody temperature—that healthcare professionals use in evaluating a patient's health. Normal resting blood pressure in an adult is approximately 120 millimetres of mercury (16 kPa) systolic over 80 millimetres of mercury (11 kPa) diastolic, denoted as "120/80 mmHg". Globally, the average blood pressure, age standardized, has remained about the same since 1975 to the present, at approximately 127/79 mmHg in men and 122/77 mmHg in women, although these average data mask significantly diverging regional trends.[3]

Traditionally, a health-care worker measured blood pressure non-invasively byauscultation(listening) through astethoscopefor sounds in one arm'sarteryas the artery is squeezed, closer to the heart, by ananeroid gaugeor amercury-tubesphygmomanometer.[4]Auscultation is still generally considered to be the gold standard of accuracy for non-invasive blood pressure readings in clinic.[5]However, semi-automated methods have become common, largely due to concerns about potential mercury toxicity,[6]although cost, ease of use and applicability toambulatory blood pressureor home blood pressure measurements have also influenced this trend.[7]Early automated alternatives to mercury-tube sphygmomanometers were often seriously inaccurate, but modern devices validated to international standards achieve an average difference between two standardized reading methods of 5 mm Hg or less, and astandard deviationof less than 8 mm Hg.[7]Most of these semi-automated methods measure blood pressure using oscillometry (measurement by a pressure transducer in the cuff of the device of small oscillations of intra-cuff pressure accompanying heartbeat-induced changes in the volume of each pulse).[8]

Blood pressure is influenced bycardiac output,systemic vascular resistance,blood volume andarterial stiffness,and varies depending on person's situation, emotional state, activity and relative health or disease state. In the short term, blood pressure isregulatedbybaroreceptors,which act via the brain to influence thenervousand theendocrinesystems.

Blood pressure that is too low is calledhypotension,pressure that is consistently too high is calledhypertension,and normal pressure is called normotension.[9]Both hypertension and hypotension have many causes and may be of sudden onset or of long duration. Long-term hypertension is a risk factor for many diseases, includingstroke,heart disease,andkidney failure.Long-term hypertension is more common than long-term hypotension.

Classification, normal and abnormal values

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Systemic arterial pressure

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Blood pressure measurements can be influenced by circumstances of measurement.[10]Guidelines use different thresholds for office (also known as clinic), home (when the person measures their own blood pressure at home), andambulatory blood pressure(using an automated device over a 24-hour period).[10]

Blood pressure classifications
Categories Systolic blood pressure,mmHg and/or Diastolic blood pressure,mmHg
Method Office Home 24hambulatory Office Home 24h ambulatory
American College of Cardiology/American Heart Association(2017)[11]
Normal <120 <120 <115 and <80 <80 <75
Elevated 120–129 120–129 115–124 and <80 <80 <75
Hypertension, stage 1 130–139 130–134 125–129 or 80–89 80–84 75–79
Hypertension, stage 2 ≥140 ≥135 ≥130 or ≥90 ≥85 ≥80
European Society of Cardiology(2024)[10]
Non-elevated <120 <120 <115 and <70 <70 <65
Elevated 120–139 120–134 115–129 and 70–89 70–84 65–79
Hypertension ≥140 ≥135 ≥130 or ≥90 ≥85 ≥80
European Society of Hypertension/International Society of Hypertension(2023)[12]
Optimal <120 and <80
Normal 120–129 and/or 80–84
High normal 130–139 and/or 85–89
Hypertension, grade 1 140–159 ≥135 ≥130 and/or 90–99 ≥85 ≥80
Hypertension, grade 2 160–179 and/or 100–109
Hypertension, grade 3 ≥180 and/or ≥110

The risk of cardiovascular disease increases progressively above 90 mmHg, especially among women.[10]

Observational studies demonstrate that people who maintain arterial pressures at the low end of these pressure ranges have much better long-term cardiovascular health. There is an ongoing medical debate over what is the optimal level of blood pressure to target when using drugs to lower blood pressure with hypertension, particularly in older people.[13]

Blood pressure fluctuates from minute to minute and normally shows a circadian rhythm over a 24-hour period,[14]with highest readings in the early morning and evenings and lowest readings at night.[15][16]Loss of the normal fall in blood pressure at night is associated with a greater future risk of cardiovascular disease and there is evidence that night-time blood pressure is a stronger predictor of cardiovascular events than day-time blood pressure.[17]Blood pressure varies over longer time periods (months to years) and this variability predicts adverse outcomes.[18]Blood pressure also changes in response to temperature, noise, emotionalstress,consumption of food or liquid, dietary factors, physical activity, changes in posture (such asstanding-up),drugs,and disease.[19]The variability in blood pressure and the better predictive value of ambulatory blood pressure measurements has led some authorities, such as the National Institute for Health and Care Excellence (NICE) in the UK, to advocate for the use of ambulatory blood pressure as the preferred method for diagnosis of hypertension.[20]

A digitalsphygmomanometerused for measuring blood pressure

Various other factors, such as age andsex,also influence a person's blood pressure. Differences between left-arm and right-arm blood pressure measurements tend to be small. However, occasionally there is a consistent difference greater than 10 mmHg which may need further investigation, e.g. forperipheral arterial disease,obstructive arterial diseaseoraortic dissection.[21][22][23][24]

There is no accepted diagnostic standard for hypotension, although pressures less than 90/60 are commonly regarded as hypotensive.[25]In practice blood pressure is considered too low only ifsymptomsare present.[26]

Systemic arterial pressure and age

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Fetal blood pressure

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Inpregnancy,it is the fetal heart and not the mother's heart that builds up the fetal blood pressure to drive blood through the fetal circulation. The blood pressure in the fetal aorta is approximately 30 mmHg at 20 weeks of gestation, and increases to approximately 45 mmHg at 40 weeks of gestation.[27]

The average blood pressure for full-term infants:[28]

  • Systolic 65–95 mmHg
  • Diastolic 30–60 mmHg

Childhood

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Reference rangesfor blood pressure (BP) in children[29]
Stage Approximate age Systolic BP,
mmHg
Diastolic BP,
mmHg
Infants 0–12 months 75–100 50–70
Toddlers and preschoolers 1–5 years 80–110 50–80
School age 6–12 years 85–120 50–80
Adolescents 13–18 years 95–140 60–90

In children the normal ranges for blood pressure are lower than for adults and depend on height.[30]Reference blood pressure values have been developed for children in different countries, based on the distribution of blood pressure in children of these countries.[31]

Aging adults

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In adults in most societies, systolic blood pressure tends to rise from early adulthood onward, up to at least age 70;[32][33]diastolic pressure tends to begin to rise at the same time but start to fall earlier in mid-life, approximately age 55.[33]Mean blood pressure rises from early adulthood, plateauing in mid-life, while pulse pressure rises quite markedly after the age of 40. Consequently, in many older people, systolic blood pressure often exceeds the normal adult range,[33]if the diastolic pressure is in the normal range this is termedisolated systolic hypertension.The rise in pulse pressure with age is attributed to increasedstiffness of the arteries.[34]An age-related rise in blood pressure is not considered healthy and is not observed in some isolated unacculturated communities.[35]

Systemic venous pressure

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Site Normal
pressure range
(inmmHg)[36]
Central venous pressure 3–8
Right ventricular pressure systolic 15–30
diastolic 3–8
Pulmonary artery pressure systolic 15–30
diastolic 4–12
Pulmonary vein/

Pulmonary capillary wedge pressure

2–15
Left ventricular pressure systolic 100–140
diastolic 3–12

Blood pressure generally refers to the arterial pressure in thesystemic circulation.However, measurement of pressures in the venous system and thepulmonary vesselsplays an important role inintensive care medicinebut requires invasive measurement of pressure using acatheter.

Venous pressure is the vascular pressure in aveinor in theatria of the heart.It is much lower than arterial pressure, with common values of 5 mmHg in theright atriumand 8 mmHg in the left atrium.

Variants of venous pressure include:

Pulmonary pressure

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Normally, the pressure in thepulmonary arteryis about 15 mmHg at rest.[40]

Increased blood pressure in thecapillariesof the lung causespulmonary hypertension,leading to interstitialedemaif the pressure increases to above 20 mmHg, and topulmonary edemaat pressures above 25 mmHg.[41]

Aortic pressure

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Aortic pressure,also called central aortic blood pressure, or central blood pressure, is the blood pressure at the root of theaorta.Elevated aortic pressure has been found to be a more accurate predictor of both cardiovascular events and mortality, as well as structural changes in the heart, than has peripheral blood pressure (such as measured through thebrachial artery).[42][43]Traditionally it involved an invasive procedure to measure aortic pressure, but now there are non-invasive methods of measuring it indirectly without a significant margin of error.[44][45]

Certain researchers have argued for physicians to begin using aortic pressure, as opposed to peripheral blood pressure, as a guide for clinical decisions.[46][43]The way antihypertensive drugs impact peripheral blood pressure can often be very different from the way they impact central aortic pressure.[47]

Mean systemic pressure

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If the heart is stopped, blood pressure falls, but it does not fall to zero. The remaining pressure measured after cessation of the heart beat and redistribution of blood throughout the circulation is termed the mean systemic pressure or mean circulatory filling pressure;[48]typically this is proximally ~7 mmHg.[48]

Disorders of blood pressure

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Disorders of blood pressure control includehigh blood pressure,low blood pressure,and blood pressure that shows excessive or maladaptive fluctuation.

High blood pressure

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Overview of main complications of persistent high blood pressure.[49]

Arterial hypertensioncan be an indicator of other problems and may have long-term adverse effects. Sometimes it can be an acute problem, such as in ahypertensive emergencywhen blood pressure is more than 180/120 mmHg.[49]

Levels of arterial pressure put mechanical stress on the arterial walls. Higher pressures increase heart workload and progression of unhealthy tissue growth (atheroma) that develops within the walls of arteries. The higher the pressure, the more stress that is present and the more atheroma tend to progress and theheart muscletends to thicken, enlarge and become weaker over time.

Persistenthypertensionis one of the risk factors forstrokes,heart attacks,heart failure,andarterial aneurysms,and is the leading cause ofchronic kidney failure.[49]Even moderate elevation of arterial pressure leads to shortenedlife expectancy.[49]At severely high pressures, mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated.[50]For people with high blood pressure, higherheart rate variability(HRV) is a risk factor foratrial fibrillation.[51]

Both highsystolicpressure and highpulse pressure(the numerical difference between systolic and diastolic pressures) are risk factors.[49]Elevated pulse pressure has been found to be a stronger independent predictor of cardiovascular events, especially in older populations, than has systolic, diastolic, or mean arterial pressure.[52][53][54][55]In some cases, it appears that a decrease in excessive diastolic pressure can actually increase risk, probably due to the increased difference between systolic and diastolic pressures (ie. widened pulse pressure). If systolic blood pressure is elevated (>140 mmHg) with a normal diastolic blood pressure (<90 mmHg), it is calledisolated systolic hypertensionand may present a health concern.[49][56]According to the 2017[57]American Heart Association blood pressure guidelines state that a systolic blood pressure of 130–139 mmHg with a diastolic pressure of 80–89 mmHg is "stage one hypertension".[49]

For those withheart valveregurgitation, a change in its severity may be associated with a change in diastolic pressure. In a study of people with heart valve regurgitation that compared measurements two weeks apart for each person, there was an increased severity ofaorticandmitral regurgitationwhen diastolic blood pressure increased, whereas when diastolic blood pressure decreased, there was a decreased severity.[58]

Low blood pressure

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Blood pressure that is too low is known ashypotension.This is a medical concern if it causes signs or symptoms, such as dizziness, fainting, or in extreme cases in medical emergencies,circulatory shock.[59]Causes of low arterial pressure includesepsis,hypovolemia,bleeding,cardiogenic shock,reflex syncope,hormonalabnormalities such asAddison's disease,eating disorders– particularlyanorexia nervosaandbulimia.[60]

Orthostatic hypotension

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A large fall in blood pressure upon standing (typically a systolic/diastolic blood pressure decrease of >20/10 mmHg) is termedorthostatic hypotension(postural hypotension) and represents a failure of the body to compensate for the effect ofgravityon the circulation. Standing results in an increasedhydrostaticpressure in the blood vessels of the lower limbs. The consequent distension of the veins below thediaphragm(venous pooling) causes ~500 ml of blood to be relocated from the chest and upper body. This results in a rapid decrease in central blood volume and a reduction of ventricularpreloadwhich in turn reduces stroke volume, and mean arterial pressure. Normally this is compensated for by multiple mechanisms, including activation of theautonomic nervous systemwhich increasesheart rate,myocardial contractilityand systemic arterialvasoconstrictionto preserve blood pressure and elicitsvenousvasoconstriction to decrease venouscompliance.Decreased venous compliance also results from an intrinsicmyogenicincrease in venoussmooth muscletone in response to the elevated pressure in the veins of the lower body.

Other compensatory mechanisms include the veno-arteriolaraxon reflex,the 'skeletal muscle pump' and 'respiratory pump'. Together these mechanisms normally stabilize blood pressure within a minute or less.[61]If these compensatory mechanisms fail and arterial pressure and bloodflowdecrease beyond a certain point, theperfusionof the brain becomes critically compromised (i.e., the blood supply is not sufficient), causinglightheadedness,dizziness,weakness orfainting.[62]Usually this failure of compensation is due to disease, or drugs that affect thesympathetic nervous system.[61]A similar effect is observed following the experience of excessive gravitational forces (G-loading), such as routinely experienced by aerobatic or combat pilots 'pulling Gs' where the extreme hydrostatic pressures exceed the ability of the body's compensatory mechanisms.

Variable or fluctuating blood pressure

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Some fluctuation or variation in blood pressure is normal. Variation in blood pressure that is significantly greater than the norm is known aslabile hypertensionand is associated with increased risk of cardiovascular disease[63]brain small vessel disease,[64]and dementia[65]independent of the average blood pressure level. Recent evidence fromclinical trialshas also linked variation in blood pressure to mortality,[66][67]stroke,[68]heart failure,[69]and cardiac changes that may give rise to heart failure.[70]These data have prompted discussion of whether excessive variation in blood pressure should be treated, even among normotensive older adults.[71]

Older individuals and those who had received blood pressure medications are more likely to exhibit larger fluctuations in pressure,[72]and there is some evidence that different antihypertensive agents have different effects on blood pressure variability;[65]whether these differences translate to benefits in outcome is uncertain.[65]

Physiology

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Cardiac systole and diastole
Blood flow velocity waveforms in the central retinal artery (red) and vein (blue), measured bylaser Doppler imagingin the eye fundus of a healthy volunteer.
Schematic of pressures in the circulation

During each heartbeat, blood pressure varies between a maximum (systolic) and a minimum (diastolic) pressure.[73][unreliable medical source]The blood pressure in the circulation is principally due to the pumping action of the heart.[74]However, blood pressure is also regulated by neural regulation from the brain (seeHypertension and the brain), as well as osmotic regulation from the kidney. Differences in mean blood pressure drive the flow of blood around the circulation. The rate of mean blood flow depends on both blood pressure and the resistance to flow presented by the blood vessels. In the absence ofhydrostaticeffects (e.g. standing), mean blood pressure decreases as thecirculating bloodmoves away from the heart through arteries andcapillariesdue toviscouslosses of energy. Mean blood pressure drops over the whole circulation, although most of the fall occurs along the small arteries andarterioles.[75]Pulsatility also diminishes in the smaller elements of the arterial circulation, although some transmitted pulsatility is observed in capillaries.[76]Gravity affects blood pressure via hydrostatic forces (e.g., during standing), and valves in veins,breathing,and pumping from contraction of skeletal muscles also influence blood pressure, particularly in veins.[74]

Hemodynamics

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A simple view of thehemodynamicsof systemic arterial pressure is based aroundmean arterial pressure(MAP) and pulse pressure. Most influences on blood pressure can be understood in terms of their effect oncardiac output,[77]systemic vascular resistance,orarterial stiffness(the inverse of arterial compliance). Cardiac output is the product of stroke volume and heart rate. Stroke volume is influenced by 1) theend-diastolic volumeor filling pressure of the ventricle acting via theFrank–Starling mechanism—this is influenced byblood volume;2)cardiac contractility;and 3)afterload,the impedance to blood flow presented by the circulation.[78]In the short-term, the greater the blood volume, the higher the cardiac output. This has been proposed as an explanation of the relationship between high dietary salt intake and increased blood pressure; however, responses to increased dietary sodium intake vary between individuals and are highly dependent on autonomic nervous system responses and therenin–angiotensin system,[79][80][81]changes inplasma osmolaritymay also be important.[82]In the longer-term the relationship between volume and blood pressure is more complex.[83]In simple terms, systemic vascular resistance is mainly determined by the caliber of small arteries and arterioles. The resistance attributable to a blood vessel depends on its radius as described by theHagen-Poiseuille's equation(resistance∝1/radius4). Hence, the smaller the radius, the higher the resistance. Other physical factors that affect resistance include: vessel length (the longer the vessel, the higher the resistance), blood viscosity (the higher the viscosity, the higher the resistance)[84]and the number of vessels, particularly the smaller numerous, arterioles and capillaries. The presence of a severe arterialstenosisincreases resistance to flow, however this increase in resistance rarely increases systemic blood pressure because its contribution to total systemic resistance is small, although it may profoundly decrease downstream flow.[85]Substances calledvasoconstrictorsreduce the caliber of blood vessels, thereby increasing blood pressure.Vasodilators(such asnitroglycerin) increase the caliber of blood vessels, thereby decreasing arterial pressure. In the longer term a process termed remodeling also contributes to changing the caliber of small blood vessels and influencing resistance and reactivity to vasoactive agents.[86][87]Reductions in capillary density, termed capillary rarefaction, may also contribute to increased resistance in some circumstances.[88]

In practice, each individual's autonomic nervous system and other systems regulating blood pressure, notably the kidney,[89]respond to and regulate all these factors so that, although the above issues are important, they rarely act in isolation and the actual arterial pressure response of a given individual can vary widely in the short and long term.

Pulse pressure

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A schematic representation of the arterial pressure waveform over one cardiac cycle. The notch in the curve is associated with closing of the aortic valve.

The pulse pressure is the difference between the measured systolic and diastolic pressures,[90]

The pulse pressure is a consequence of the pulsatile nature of thecardiac output,i.e. the heartbeat. The magnitude of the pulse pressure is usually attributed to the interaction of thestroke volumeof the heart, the compliance (ability to expand) of the arterial system—largely attributable to theaortaand large elastic arteries—and theresistanceto flow in thearterial tree.[90]

Clinical significance of pulse pressure

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A healthy pulse pressure is around 40 mmHg.[1]A pulse pressure that is consistently 60 mmHg or greater is likely to be associated with disease, and a pulse pressure of 50 mmHg or more increases the risk ofcardiovascular diseaseas well as other complications such as eye and kidney disease.[52]Pulse pressure is considered low if it is less than 25% of the systolic. (For example, if the systolic pressure is 120 mmHg, then the pulse pressure would be considered low if it is less than 30 mmHg, since 30 is 25% of 120.)[91]A very low pulse pressure can be a symptom of disorders such ascongestive heart failure.[52]

Elevated pulse pressure has been found to be a stronger independent predictor of cardiovascular events, especially in older populations, than has systolic, diastolic, or mean arterial pressure.[52][53]This increased risk exists for both men and women and even when no other cardiovascular risk factors are present. The increased risk also exists even in cases in which diastolic pressure decreases over time while systolic remains steady.[55][54]

Ameta-analysisin 2000 showed that a 10 mmHg increase in pulse pressure was associated with a 20% increased risk of cardiovascular mortality, and a 13% increase in risk for all coronary end points. The study authors also noted that, while risks of cardiovascular end points do increase with higher systolic pressures, at any given systolic blood pressure the risk of major cardiovascular end points increases, rather than decreases, with lower diastolic levels. This suggests that interventions that lower diastolic pressure without also lowering systolic pressure (and thus lowering pulse pressure) could actually be counterproductive.[92]There are no drugs currently approved to lower pulse pressure, although some antihypertensive drugs may modestly lower pulse pressure, while in some cases a drug that lowers overall blood pressure may actually have the counterproductive side effect of raising pulse pressure.[93]

Pulse pressure can both widen or narrow in people withsepsisdepending on the degree ofhemodynamiccompromise. A pulse pressure of over 70 mmHg in sepsis is correlated with an increased chance of survival and a more positive response toIV fluids.[94][95]

Mean arterial pressure

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Mean arterial pressure(MAP) is the average of blood pressure over acardiac cycleand is determined by thecardiac output(CO),systemic vascular resistance(SVR), andcentral venous pressure(CVP):[2][96][97]

In practice, the contribution of CVP (which is small) is generally ignored and so

MAP is often estimated from measurements of the systolic pressure,and the diastolic pressure,[97]using the equation:

wherek= 0.333 although other values forkhave been advocated.[98][99]

Regulation of blood pressure

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Theendogenous,homeostaticregulation of arterial pressure is not completely understood, but the following mechanisms of regulating arterial pressure have been well-characterized:

These different mechanisms are not necessarily independent of each other, as indicated by the link between the RAS and aldosterone release. When blood pressure falls many physiological cascades commence in order to return the blood pressure to a more appropriate level.

  1. The blood pressure fall is detected by a decrease in blood flow and thus a decrease inglomerular filtration rate(GFR).
  2. Decrease in GFR is sensed as a decrease in Na+levels by themacula densa.
  3. The macula densa causes an increase in Na+reabsorption, which causes water to follow in viaosmosisand leads to an ultimate increase inplasmavolume. Further, the macula densa releases adenosine which causes constriction of the afferent arterioles.
  4. At the same time, thejuxtaglomerular cellssense the decrease in blood pressure and releaserenin.
  5. Renin convertsangiotensinogen(inactive form) toangiotensin I(active form).
  6. Angiotensin I flows in the bloodstream until it reaches the capillaries of the lungs whereangiotensin-converting enzyme(ACE) acts on it to convert it intoangiotensin II.
  7. Angiotensin II is a vasoconstrictor that will increase blood flow to the heart and subsequently the preload, ultimately increasing thecardiac output.
  8. Angiotensin II also causes an increase in the release ofaldosteronefrom theadrenal glands.
  9. Aldosterone further increases the Na+and H2O reabsorption in thedistal convoluted tubuleof thenephron.

The RAS is targeted pharmacologically byACE inhibitorsandangiotensin II receptor antagonists(also known as angiotensin receptor blockers; ARB). The aldosterone system is directly targeted byaldosterone antagonists.The fluid retention may be targeted bydiuretics;the antihypertensive effect of diuretics is due to its effect on blood volume. Generally, the baroreceptor reflex is not targeted inhypertensionbecause if blocked, individuals may experienceorthostatic hypotensionandfainting.

Measurement

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Taking blood pressure with a sphygmomanometer
Measuring systolic and diastolic blood pressure using a mercury sphygmomanometer

Arterial pressure is most commonly measured via asphygmomanometer,which uses the height of a column of mercury, or ananeroid gauge,to reflect the blood pressure by auscultation.[4]The most common automated blood pressure measurement technique is based on theoscillometricmethod.[103]Fully automated oscillometric measurement has been available since 1981.[104]This principle has recently been used to measure blood pressure with a smartphone.[105]Measuring pressureinvasively,by penetrating the arterial wall to take the measurement, is much less common and usually restricted to a hospital setting. Novel methods to measure blood pressure without penetrating the arterial wall, and without applying any pressure on patient's body are being explored,[106]for example, cuffless measurements that uses only optical sensors.[107]

In office blood pressure measurement,terminal digit preferenceis common. According to one study, approximately 40% of recorded measurements ended with the digit zero, whereas "without bias, 10%–20% of measurements are expected to end in zero"[108]

In animals

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Blood pressure levels in non-human mammals may vary depending on the species. Heart rate differs markedly, largely depending on the size of the animal (larger animals have slower heart rates).[109]The giraffe has a distinctly high arterial pressure of about 190 mm Hg, enabling blood perfusion through the 2 metres (6 ft 7 in)-long neck to the head.[110]In other species subjected to orthostatic blood pressure, such asarborealsnakes, blood pressure is higher than in non-arboreal snakes.[111]A heart near to the head (short heart-to-head distance) and a long tail with tightintegumentfavor blood perfusion to the head.[112][113]

As in humans, blood pressure in animals differs by age, sex, time of day, and environmental circumstances:[114][115]measurements made in laboratories or under anesthesia may not be representative of values under free-living conditions. Rats, mice, dogs and rabbits have been used extensively to study the regulation of blood pressure.[116]

Blood pressure and heart rate of various mammals[114]
Species Blood pressure
mm Hg
Heart rate
beats per minute
Systolic Diastolic
Calves 140 70 75–146
Cats 155 68 100–259
Dogs 161 51 62–170
Goats 140 90 80–120
Guinea-pigs 140 90 240–300
Mice 120 75 580–680
Pigs 169 55 74–116
Rabbits 118 67 205–306
Rats 153 51 305–500
Rhesus monkeys 160 125 180–210
Sheep 140 80 63–210

Hypertension in cats and dogs

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Hypertension in cats and dogs is generally diagnosed if the blood pressure is greater than 150 mm Hg (systolic),[117]althoughsight houndshave higher blood pressures than most other dog breeds; a systolic pressure greater than 180 mmHg is considered abnormal in these dogs.[118]

See also

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References

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  1. ^abHoman TD, Bordes SJ, Cichowski E (12 July 2022)."Physiology, Pulse Pressure".StatPearls [Internet].Treasure Island (FL): StatPearls Publishing.PMID29494015.Retrieved2019-07-21– via NCBI Bookshelf.
  2. ^abMayet J, Hughes A (September 2003)."Cardiac and vascular pathophysiology in hypertension".Heart.89(9): 1104–1109.doi:10.1136/heart.89.9.1104.PMC1767863.PMID12923045.
  3. ^Zhou B, Bentham J, Di Cesare M, Bixby H, Danaei G, Cowan MJ, et al. (NCD Risk Factor Collaboration (NCD-RisC)) (January 2017)."Worldwide trends in blood pressure from 1975 to 2015: a pooled analysis of 1479 population-based measurement studies with 19·1 million participants".Lancet.389(10064): 37–55.doi:10.1016/S0140-6736(16)31919-5.PMC5220163.PMID27863813.
  4. ^abBooth J (November 1977)."A short history of blood pressure measurement".Proceedings of the Royal Society of Medicine.70(11): 793–799.doi:10.1177/003591577707001112.PMC1543468.PMID341169.
  5. ^Grim CE, Grim CM (March 2016). "Auscultatory BP: still the gold standard".Journal of the American Society of Hypertension.10(3): 191–193.doi:10.1016/j.jash.2016.01.004.PMID26839183.
  6. ^O'Brien E (January 2001)."Blood pressure measurement is changing!".Heart.85(1): 3–5.doi:10.1136/heart.85.1.3.PMC1729570.PMID11119446.
  7. ^abOgedegbe G, Pickering T (November 2010)."Principles and techniques of blood pressure measurement".Cardiology Clinics.28(4): 571–586.doi:10.1016/j.ccl.2010.07.006.PMC3639494.PMID20937442.
  8. ^Alpert BS, Quinn D, Gallick D (December 2014). "Oscillometric blood pressure: a review for clinicians".Journal of the American Society of Hypertension.8(12): 930–938.doi:10.1016/j.jash.2014.08.014.PMID25492837.
  9. ^Newman WA, ed. (2012).Dorland's illustrated medical dictionary(32nd ed.). Philadelphia, PA: Saunders/Elsevier.ISBN978-1-4160-6257-8.OCLC706780870.
  10. ^abcdMcEvoy, John William; McCarthy, Cian P; Bruno, Rosa Maria; Brouwers, Sofie; Canavan, Michelle D; et al. (2024-08-30)."2024 ESC Guidelines for the management of elevated blood pressure and hypertension: Developed by the task force on the management of elevated blood pressure and hypertension of the European Society of Cardiology (ESC) and endorsed by the European Society of Endocrinology (ESE) and the European Stroke Organisation (ESO)".European Heart Journal.doi:10.1093/eurheartj/ehae178.ISSN0195-668X.
  11. ^Whelton, Paul K; Carey, Robert M; Mancia, Giuseppe; Kreutz, Reinhold; Bundy, Joshua D; Williams, Bryan (2022-09-14)."Harmonization of the American College of Cardiology/American Heart Association and European Society of Cardiology/European Society of Hypertension Blood Pressure/Hypertension Guidelines".European Heart Journal.43(35): 3302–3311.doi:10.1093/eurheartj/ehac432.ISSN0195-668X.PMC9470378.PMID36100239.
  12. ^Mancia, Giuseppe; Kreutz, Reinhold; Brunström, Mattias; Burnier, Michel; Grassi, Guido; et al. (2023-12-01)."2023 ESH Guidelines for the management of arterial hypertension The Task Force for the management of arterial hypertension of the European Society of Hypertension: Endorsed by the International Society of Hypertension (ISH) and the European Renal Association (ERA)".Journal of Hypertension.41(12): 1874–2071.doi:10.1097/HJH.0000000000003480.hdl:11379/603005.ISSN1473-5598.PMID37345492.
  13. ^Yusuf S, Lonn E (November 2016). "The SPRINT and the HOPE-3 Trial in the Context of Other Blood Pressure-Lowering Trials".JAMA Cardiology.1(8): 857–858.doi:10.1001/jamacardio.2016.2169.PMID27602555.
  14. ^Smolensky MH, Hermida RC, Portaluppi F (June 2017). "Circadian mechanisms of 24-hour blood pressure regulation and patterning".Sleep Medicine Reviews.33:4–16.doi:10.1016/j.smrv.2016.02.003.PMID27076261.
  15. ^van Berge-Landry HM, Bovbjerg DH, James GD (October 2008)."Relationship between waking-sleep blood pressure and catecholamine changes in African-American and European-American women".Blood Pressure Monitoring.13(5): 257–262.doi:10.1097/MBP.0b013e3283078f45.PMC2655229.PMID18799950.Table2: Comparison of ambulatory blood pressures and urinary norepinephrine and epinephrine excretion measured at work, home, and during sleep between European–American (n = 110) and African–American (n = 51) women
  16. ^van Berge-Landry HM, Bovbjerg DH, James GD (October 2008)."Relationship between waking-sleep blood pressure and catecholamine changes in African-American and European-American women".Blood Pressure Monitoring.13(5): 257–262.doi:10.1097/MBP.0b013e3283078f45.PMC2655229.PMID18799950.NIHMS90092.
  17. ^Hansen TW, Li Y, Boggia J, Thijs L, Richart T, Staessen JA (January 2011)."Predictive role of the nighttime blood pressure".Hypertension.57(1): 3–10.doi:10.1161/HYPERTENSIONAHA.109.133900.PMID21079049.
  18. ^Rothwell PM (June 2011). "Does blood pressure variability modulate cardiovascular risk?".Current Hypertension Reports.13(3): 177–186.doi:10.1007/s11906-011-0201-3.PMID21465141.S2CID207331784.
  19. ^Engel BT, Blümchen G, eds. (1992).Temporal Variations of the Cardiovascular System.Berlin, Heidelberg: Springer Berlin Heidelberg.ISBN978-3-662-02748-6.OCLC851391490.
  20. ^National Clinical Guideline Centre (UK) (2011).Hypertension: The Clinical Management of Primary Hypertension in Adults: Update of Clinical Guidelines 18 and 34.National Institute for Health and Clinical Excellence: Guidance. London: Royal College of Physicians (UK).PMID22855971.Archivedfrom the original on 2022-08-12.Retrieved2019-01-28.
  21. ^Eguchi K, Yacoub M, Jhalani J, Gerin W, Schwartz JE, Pickering TG (February 2007)."Consistency of blood pressure differences between the left and right arms".Archives of Internal Medicine.167(4): 388–393.doi:10.1001/archinte.167.4.388.PMID17325301.
  22. ^Agarwal R, Bunaye Z, Bekele DM (March 2008). "Prognostic significance of between-arm blood pressure differences".Hypertension.51(3): 657–662.CiteSeerX10.1.1.540.5836.doi:10.1161/HYPERTENSIONAHA.107.104943.PMID18212263.S2CID1101762.
  23. ^Clark CE, Campbell JL, Evans PH, Millward A (December 2006)."Prevalence and clinical implications of the inter-arm blood pressure difference: A systematic review".Journal of Human Hypertension.20(12): 923–931.doi:10.1038/sj.jhh.1002093.PMID17036043.
  24. ^Clark CE, Warren FC, Boddy K, McDonagh ST, Moore SF, Goddard J, et al. (February 2021)."Associations Between Systolic Interarm Differences in Blood Pressure and Cardiovascular Disease Outcomes and Mortality: Individual Participant Data Meta-Analysis, Development and Validation of a Prognostic Algorithm: The INTERPRESS-IPD Collaboration".Hypertension.77(2): 650–661.doi:10.1161/HYPERTENSIONAHA.120.15997.PMC7803446.PMID33342236.
  25. ^Sharma S, Bhattacharya PT (2018)."Hypotension".StatPearls.StatPearls Publishing.PMID29763136.Archivedfrom the original on 2020-03-17.Retrieved2018-12-23.
  26. ^Mayo Clinic staff (2009-05-23)."Low blood pressure (hypotension) – Causes".MayoClinic.Mayo Foundation for Medical Education and Research.Archivedfrom the original on 2021-11-17.Retrieved2010-10-19.
  27. ^Struijk PC, Mathews VJ, Loupas T, Stewart PA, Clark EB, Steegers EA, Wladimiroff JW (October 2008)."Blood pressure estimation in the human fetal descending aorta".Ultrasound in Obstetrics & Gynecology.32(5): 673–681.doi:10.1002/uog.6137.PMID18816497.S2CID23575926.
  28. ^Sharon SM, Emily SM (2006).Foundations of Maternal-Newborn Nursing(4th ed.). Philadelphia: Elsevier. p. 476.
  29. ^Pediatric Age SpecificArchived2017-05-16 at theWayback Machine,p. 6. Revised 6/10. By Theresa Kirkpatrick and Kateri Tobias. UCLA Health System
  30. ^National Heart Lung and Blood Institute."Blood pressure tables for children and adolescents".Archived fromthe originalon 2014-06-18.Retrieved2008-09-23.(The median blood pressure is given by the 50th percentile and hypertension is defined by the95th percentilefor a given age, height, and sex.)
  31. ^Chiolero A (March 2014)."The quest for blood pressure reference values in children".Journal of Hypertension.32(3): 477–479.doi:10.1097/HJH.0000000000000109.PMID24477093.S2CID1949314.
  32. ^Wills AK, Lawlor DA, Matthews FE, Sayer AA, Bakra E, Ben-Shlomo Y, et al. (June 2011)."Life course trajectories of systolic blood pressure using longitudinal data from eight UK cohorts".PLOS Medicine.8(6): e1000440.doi:10.1371/journal.pmed.1000440.PMC3114857.PMID21695075.
  33. ^abcFranklin SS, Gustin W, Wong ND, Larson MG, Weber MA, Kannel WB, Levy D (July 1997). "Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study".Circulation.96(1): 308–315.doi:10.1161/01.CIR.96.1.308.PMID9236450.S2CID40209177.
  34. ^Franklin SS (2008-05-01). "Beyond blood pressure: Arterial stiffness as a new biomarker of cardiovascular disease".Journal of the American Society of Hypertension.2(3): 140–151.doi:10.1016/j.jash.2007.09.002.PMID20409896.
  35. ^Gurven M, Blackwell AD, Rodríguez DE, Stieglitz J, Kaplan H (July 2012)."Does blood pressure inevitably rise with age?: longitudinal evidence among forager-horticulturalists".Hypertension.60(1): 25–33.doi:10.1161/HYPERTENSIONAHA.111.189100.PMC3392307.PMID22700319.
  36. ^Table 30-1 in:Goers TA, Klingensmith ME, Chen LE, Glasgow SC (2008).The Washington Manual of Surgery.Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins.ISBN978-0-7817-7447-5.
  37. ^"Central Venous Catheter Physiology".Archived fromthe originalon 2008-08-21.Retrieved2009-02-27.
  38. ^Tkachenko BI, Evlakhov VI, Poyasov IZ (October 2002). "Independence of changes in right atrial pressure and central venous pressure".Bulletin of Experimental Biology and Medicine.134(4): 318–320.doi:10.1023/A:1021931508946.PMID12533747.S2CID23726657.
  39. ^"Esophageal Varices: Article Excerpt by: Samy A Azer".eMedicine.Archivedfrom the original on 2008-10-07.Retrieved2011-08-22.
  40. ^"What Is Pulmonary Hypertension?".From Diseases and Conditions Index (DCI).National Heart, Lung, and Blood Institute. September 2008.Archivedfrom the original on 27 April 2012.Retrieved6 April2009.
  41. ^Adair OV (2001). "Chapter 41".Cardiology secrets(2nd ed.). Philadelphia: Hanley & Belfus. p. 210.ISBN978-1-56053-420-4.
  42. ^Roman, Mary J.; Devereux, Richard B.; Kizer, Jorge R.; Lee, Elisa T.; Galloway, James M.; Ali, Tauqeer; Umans, Jason G.; Howard, Barbara V. (2007). "Central Pressure More Strongly Relates to Vascular Disease and Outcome Than Does Brachial Pressure".Hypertension.50(1). Ovid Technologies (Wolters Kluwer Health): 197–203.doi:10.1161/hypertensionaha.107.089078.ISSN0194-911X.
  43. ^abKesten, Steven; Qasem, Ahmad; Avolio, Alberto (2022-10-20)."Viewpoint: The Case for Non-Invasive Central Aortic Pressure Monitoring in the Management of Hypertension".Artery Research.28(4): 128–139.doi:10.1007/s44200-022-00023-z.ISSN1876-4401.
  44. ^Avolio, Alberto (2008). "Central Aortic Blood Pressure and Cardiovascular Risk: A Paradigm Shift?".Hypertension.51(6): 1470–1471.doi:10.1161/HYPERTENSIONAHA.107.108910.ISSN0194-911X.
  45. ^Chen, Chen-Huan; Nevo, Erez; Fetics, Barry; Pak, Peter H.; Yin, Frank C.P.; Maughan, W. Lowell; Kass, David A. (1997). "Estimation of Central Aortic Pressure Waveform by Mathematical Transformation of Radial Tonometry Pressure".Circulation.95(7). Ovid Technologies (Wolters Kluwer Health): 1827–1836.doi:10.1161/01.cir.95.7.1827.ISSN0009-7322.
  46. ^McEniery, Carmel M.; Cockcroft, John R.; Roman, Mary J.; Franklin, Stanley S.; Wilkinson, Ian B. (23 Jan 2014)."Central blood pressure: current evidence and clinical importance".European Heart Journal.35(26). Oxford University Press (OUP): 1719–1725.doi:10.1093/eurheartj/eht565.ISSN1522-9645.PMC4155427.
  47. ^The CAFE Investigators; CAFE Steering Committee and Writing Committee; Williams, Bryan; Lacy, Peter S.; Thom, Simon M.; Cruickshank, Kennedy; Stanton, Alice; Collier, David; Hughes, Alun D.; Thurston, H.; O’Rourke, Michael (2006-03-07). "Differential Impact of Blood Pressure–Lowering Drugs on Central Aortic Pressure and Clinical Outcomes: Principal Results of the Conduit Artery Function Evaluation (CAFE) Study".Circulation.113(9): 1213–1225.doi:10.1161/CIRCULATIONAHA.105.595496.ISSN0009-7322.
  48. ^abRothe CF (February 1993). "Mean circulatory filling pressure: its meaning and measurement".Journal of Applied Physiology.74(2): 499–509.doi:10.1152/jappl.1993.74.2.499.PMID8458763.
  49. ^abcdefg"The facts about high blood pressure".American Heart Association. 2023.Archivedfrom the original on 14 May 2023.Retrieved14 May2023.
  50. ^Guyton AC (2006).Textbook of Medical Physiology(11th ed.). Philadelphia: Elsevier Saunders. p. 220.ISBN978-0-7216-0240-0.
  51. ^Kim SH, Lim KR, Chun KJ (2022)."Higher heart rate variability as a predictor of atrial fibrillation in patients with hypertensione".Scientific Reports.12(1): 3702.doi:10.1038/s41598-022-07783-3.PMC8904557.PMID35260686.
  52. ^abcd"Pulse pressure".Cleveland Clinic. 28 July 2021.Retrieved10 February2023.
  53. ^abMitchell, Gary F.; Izzo, Joseph L.; Lacourcière, Yves; Ouellet, Jean-Pascal; Neutel, Joel; Qian, Chunlin; Kerwin, Linda J.; Block, Alan J.; Pfeffer, Marc A. (25 Jun 2002). "Omapatrilat Reduces Pulse Pressure and Proximal Aortic Stiffness in Patients With Systolic Hypertension".Circulation.105(25). Ovid Technologies (Wolters Kluwer Health): 2955–2961.doi:10.1161/01.cir.0000020500.77568.3c.ISSN0009-7322.PMID12081987.S2CID7092379.
  54. ^abBenetos, Athanase; Safar, Michel; Rudnichi, Annie; Smulyan, Harold; Richard, Jacques-Lucien; Ducimetière, Pierre; Guize, Louis (1997). "Pulse Pressure".Hypertension.30(6). Ovid Technologies (Wolters Kluwer Health): 1410–1415.doi:10.1161/01.hyp.30.6.1410.ISSN0194-911X.PMID9403561.
  55. ^abFranklin, Stanley S.; Khan, Shehzad A.; Wong, Nathan D.; Larson, Martin G.; Levy, Daniel (27 Jul 1999)."Is Pulse Pressure Useful in Predicting Risk for Coronary Heart Disease?".Circulation.100(4). Ovid Technologies (Wolters Kluwer Health): 354–360.doi:10.1161/01.cir.100.4.354.ISSN0009-7322.PMID10421594.
  56. ^"Isolated systolic hypertension: A health concern?".MayoClinic.Archivedfrom the original on 2013-12-28.Retrieved2018-01-25.
  57. ^Tan JL, Thakur K (2022)."Systolic Hypertension".StatPearls.Treasure Island (FL): StatPearls Publishing.PMID29494079.Retrieved2022-10-03.
  58. ^Gottdiener JS, Panza JA, St John Sutton M, Bannon P, Kushner H, Weissman NJ (July 2002). "Testing the test: the reliability of echocardiography in the sequential assessment of valvular regurgitation".American Heart Journal.144(1): 115–121.doi:10.1067/mhj.2002.123139.PMID12094197.
  59. ^"Diseases and conditions index – hypotension".National Heart Lung and Blood Institute. September 2008.Archivedfrom the original on 2012-04-27.Retrieved2008-09-16.
  60. ^Braunwald E, Bonow RO (2012).Braunwald's heart disease: a textbook of cardiovascular medicine(9th ed.). Philadelphia: Saunders.ISBN978-1-4377-0398-6.OCLC671465395.
  61. ^abRicci F, De Caterina R, Fedorowski A (August 2015)."Orthostatic Hypotension: Epidemiology, Prognosis, and Treatment".Journal of the American College of Cardiology.66(7): 848–860.doi:10.1016/j.jacc.2015.06.1084.PMID26271068.
  62. ^Franco Folino A (2007). "Cerebral autoregulation and syncope".Progress in Cardiovascular Diseases.50(1): 49–80.doi:10.1016/j.pcad.2007.01.001.PMID17631437.
  63. ^Stevens SL, Wood S, Koshiaris C, Law K, Glasziou P, Stevens RJ, McManus RJ (August 2016)."Blood pressure variability and cardiovascular disease: systematic review and meta-analysis".BMJ.354:i4098.doi:10.1136/bmj.i4098.PMC4979357.PMID27511067.
  64. ^Tully PJ, Yano Y, Launer LJ, Kario K, Nagai M, Mooijaart SP, et al. (January 2020)."Association Between Blood Pressure Variability and Cerebral Small-Vessel Disease: A Systematic Review and Meta-Analysis".Journal of the American Heart Association.9(1): e013841.doi:10.1161/JAHA.119.013841.PMC6988154.PMID31870233.
  65. ^abcMesserli FH, Hofstetter L, Rimoldi SF, Rexhaj E, Bangalore S (May 2019)."Risk Factor Variability and Cardiovascular Outcome: JACC Review Topic of the Week".Journal of the American College of Cardiology.73(20): 2596–2603.doi:10.1016/j.jacc.2019.02.063.PMID31118154.
  66. ^Chiriacò M, Pateras K, Virdis A, Charakida M, Kyriakopoulou D, Nannipieri M, et al. (December 2019). "Association between blood pressure variability, cardiovascular disease and mortality in type 2 diabetes: A systematic review and meta-analysis".Diabetes, Obesity & Metabolism.21(12): 2587–2598.doi:10.1111/dom.13828.hdl:11568/996646.PMID31282073.S2CID195829708.
  67. ^Nuyujukian DS, Newell MS, Zhou JJ, Koska J, Reaven PD (May 2022)."Baseline blood pressure modifies the role of blood pressure variability in mortality: Results from the ACCORD trial".Diabetes, Obesity & Metabolism.24(5): 951–955.doi:10.1111/dom.14649.PMC8986598.PMID35014154.S2CID245896131.
  68. ^Muntner P, Whittle J, Lynch AI, Colantonio LD, Simpson LM, Einhorn PT, et al. (September 2015)."Visit-to-Visit Variability of Blood Pressure and Coronary Heart Disease, Stroke, Heart Failure, and Mortality: A Cohort Study".Annals of Internal Medicine.163(5): 329–338.doi:10.7326/M14-2803.PMC5021508.PMID26215765.
  69. ^Nuyujukian DS, Koska J, Bahn G, Reaven PD, Zhou JJ (July 2020)."Blood Pressure Variability and Risk of Heart Failure in ACCORD and the VADT".Diabetes Care.43(7): 1471–1478.doi:10.2337/dc19-2540.hdl:10150/641980.PMC7305004.PMID32327422.
  70. ^Nwabuo CC, Yano Y, Moreira HT, Appiah D, Vasconcellos HD, Aghaji QN, et al. (July 2020)."Association Between Visit-to-Visit Blood Pressure Variability in Early Adulthood and Myocardial Structure and Function in Later Life".JAMA Cardiology.5(7): 795–801.doi:10.1001/jamacardio.2020.0799.PMC7160747.PMID32293640.
  71. ^Parati G, Ochoa JE, Lombardi C, Bilo G (March 2013). "Assessment and management of blood-pressure variability".Nature Reviews. Cardiology.10(3): 143–155.doi:10.1038/nrcardio.2013.1.PMID23399972.S2CID22425558.
  72. ^Brickman AM, Reitz C, Luchsinger JA, Manly JJ, Schupf N, Muraskin J, et al. (May 2010)."Long-term blood pressure fluctuation and cerebrovascular disease in an elderly cohort".Archives of Neurology.67(5): 564–569.doi:10.1001/archneurol.2010.70.PMC2917204.PMID20457955.
  73. ^"Normal Blood Pressure Ranges in Adults".svollop.2023-03-16.Archivedfrom the original on 2023-03-16.Retrieved2023-03-21.
  74. ^abCaro CG (1978).The Mechanics of The Circulation.Oxford [Oxfordshire]: Oxford University Press.ISBN978-0-19-263323-1.
  75. ^Klabunde R (2005).Cardiovascular Physiology Concepts.Lippincott Williams & Wilkins. pp. 93–94.ISBN978-0-7817-5030-1.
  76. ^Mahler F, Muheim MH, Intaglietta M, Bollinger A, Anliker M (June 1979). "Blood pressure fluctuations in human nailfold capillaries".The American Journal of Physiology.236(6): H888–H893.doi:10.1152/ajpheart.1979.236.6.H888.PMID443454.
  77. ^Guyton AC (December 1981)."The relationship of cardiac output and arterial pressure control".Circulation.64(6): 1079–1088.doi:10.1161/01.cir.64.6.1079.PMID6794930.
  78. ^Milnor WR (May 1975)."Arterial impedance as ventricular afterload".Circulation Research.36(5): 565–570.doi:10.1161/01.res.36.5.565.PMID1122568.
  79. ^Freis ED (April 1976)."Salt, volume and the prevention of hypertension".Circulation.53(4): 589–595.doi:10.1161/01.CIR.53.4.589.PMID767020.
  80. ^Caplea A, Seachrist D, Dunphy G, Ely D (April 2001). "Sodium-induced rise in blood pressure is suppressed by androgen receptor blockade".American Journal of Physiology. Heart and Circulatory Physiology.4.280(4): H1793–H1801.doi:10.1152/ajpheart.2001.280.4.H1793.PMID11247793.S2CID12069178.
  81. ^Houston MC (January 1986). "Sodium and hypertension. A review".Archives of Internal Medicine.1.146(1): 179–185.doi:10.1001/archinte.1986.00360130217028.PMID3510595.
  82. ^Kanbay M, Aslan G, Afsar B, Dagel T, Siriopol D, Kuwabara M, et al. (October 2018)."Acute effects of salt on blood pressure are mediated by serum osmolality".Journal of Clinical Hypertension.20(10): 1447–1454.doi:10.1111/jch.13374.PMC8030773.PMID30232829.
  83. ^Titze J, Luft FC (June 2017)."Speculations on salt and the genesis of arterial hypertension".Kidney International.91(6): 1324–1335.doi:10.1016/j.kint.2017.02.034.PMID28501304.
  84. ^Lee AJ (December 1997)."The role of rheological and haemostatic factors in hypertension".Journal of Human Hypertension.11(12): 767–776.doi:10.1038/sj.jhh.1000556.PMID9468002.
  85. ^Coffman JD (December 1988). "Pathophysiology of obstructive arterial disease".Herz.13(6): 343–350.PMID3061915.
  86. ^Korner PI, Angus JA (1992). "Structural determinants of vascular resistance properties in hypertension. Haemodynamic and model analysis".Journal of Vascular Research.29(4): 293–312.doi:10.1159/000158945.PMID1391553.
  87. ^Mulvany MJ (January 2012)."Small artery remodelling in hypertension".Basic & Clinical Pharmacology & Toxicology.110(1): 49–55.doi:10.1111/j.1742-7843.2011.00758.x.PMID21733124.
  88. ^de Moraes R, Tibirica E (2017). "Early Functional and Structural Microvascular Changes in Hypertension Related to Aging".Current Hypertension Reviews.13(1): 24–32.doi:10.2174/1573402113666170413095508.PMID28412915.
  89. ^Guyton AC, Coleman TG, Cowley AV, Scheel KW, Manning RD, Norman RA (May 1972). "Arterial pressure regulation. Overriding dominance of the kidneys in long-term regulation and in hypertension".The American Journal of Medicine.52(5): 584–594.doi:10.1016/0002-9343(72)90050-2.PMID4337474.
  90. ^abKlabunde RE (2007)."Cardiovascular Physiology Concepts – Pulse Pressure".Archived fromthe originalon 2009-10-18.Retrieved2008-10-02.
  91. ^Liaw SY, Scherpbier A, Klainin-Yobas P, Rethans JJ (September 2011). "A review of educational strategies to improve nurses' roles in recognizing and responding to deteriorating patients".International Nursing Review.58(3): 296–303.doi:10.1111/j.1466-7657.2011.00915.x.PMID21848774.
  92. ^Blacher J, Staessen JA, Girerd X, Gasowski J, Thijs L, Liu L, et al. (April 2000)."Pulse pressure not mean pressure determines cardiovascular risk in older hypertensive patients".Archives of Internal Medicine.160(8): 1085–1089.doi:10.1001/archinte.160.8.1085.PMID10789600.
  93. ^Cushman, William C.; Materson, Barry J.; Williams, David W.; Reda, Domenic J. (1 Oct 2001)."Pulse Pressure Changes With Six Classes of Antihypertensive Agents in a Randomized, Controlled Trial".Hypertension.38(4): 953–957.doi:10.1161/hy1001.096212.PMID11641316.
  94. ^Khilnani P, Singhi S, Lodha R, Santhanam I, Sachdev A, Chugh K, Jaishree M, Ranjit S, Ramachandran B, Ali U, Udani S, Uttam R, Deopujari S (January 2010)."Pediatric Sepsis Guidelines: Summary for resource-limited countries".Indian J Crit Care Med.14(1): 41–52.doi:10.4103/0972-5229.63029.PMC2888329.PMID20606908.
  95. ^Al-Khalisy H, Nikiforov I, Jhajj M, Kodali N, Cheriyath P (11 December 2015)."A widened pulse pressure: a potential valuable prognostic indicator of mortality in patients with sepsis. J Community Hosp Intern Med Perspect".J Community Hosp Intern Med Perspect.5(6): 29426.doi:10.3402/jchimp.v5.29426.PMC4677588.PMID26653692.
  96. ^Granger JP, Hall JE (2007). "Role of the Kidney in Hypertension".Comprehensive Hypertension.Elsevier. pp. 241–263.doi:10.1016/b978-0-323-03961-1.50026-x.ISBN978-0-323-03961-1.
  97. ^abKlabunde RE (2007)."Cardiovascular Physiology Concepts – Mean Arterial Pressure".Archived fromthe originalon 2009-10-02.Retrieved2008-09-29.
  98. ^Bos WJ, Verrij E, Vincent HH, Westerhof BE, Parati G, van Montfrans GA (April 2007). "How to assess mean blood pressure properly at the brachial artery level".Journal of Hypertension.25(4): 751–755.doi:10.1097/HJH.0b013e32803fb621.PMID17351365.S2CID23155959.
  99. ^Meaney E, Alva F, Moguel R, Meaney A, Alva J, Webel R (July 2000)."Formula and nomogram for the sphygmomanometric calculation of the mean arterial pressure".Heart.84(1): 64.doi:10.1136/heart.84.1.64.PMC1729401.PMID10862592.
  100. ^Klabunde RE (2007)."Cardiovascular Physiology Concepts – Arterial Baroreceptors".Archivedfrom the original on 2009-12-23.Retrieved2008-09-09.
  101. ^Fountain J, Lappin SL (January 2022)."Physiology, Renin Angiotensin System.".StatPearls.Treasure Island, FL: StatPearls Publishing.PMID29261862.Archivedfrom the original on 29 April 2019.Retrieved18 November2022.
  102. ^Feldman RD (January 2014)."Aldosterone and blood pressure regulation: recent milestones on the long and winding road from electrocortin to KCNJ5, GPER, and beyond".Hypertension.63(1): 19–21.doi:10.1161/HYPERTENSIONAHA.113.01251.PMID24191283.
  103. ^Forouzanfar M, Dajani HR, Groza VZ, Bolic M, Rajan S, Batkin I (2015-01-01). "Oscillometric Blood Pressure Estimation: Past, Present, and Future".IEEE Reviews in Biomedical Engineering.8:44–63.doi:10.1109/RBME.2015.2434215.PMID25993705.S2CID8940215.
  104. ^"Apparatus and method for measuring blood pressure".Archivedfrom the original on 2022-10-26.Retrieved2019-01-12– via Google patents.
  105. ^Chandrasekhar A, Kim CS, Naji M, Natarajan K, Hahn JO, Mukkamala R (March 2018)."Smartphone-based blood pressure monitoring via the oscillometric finger-pressing method".Science Translational Medicine.10(431): eaap8674.doi:10.1126/scitranslmed.aap8674.PMC6039119.PMID29515001.
  106. ^Solà J, Delgado-Gonzalo R (2019).The Handbook of Cuffless Blood Pressure Monitoring.Springer International Publishing.ISBN978-3-030-24701-0.Archivedfrom the original on 2021-06-17.Retrieved2020-01-29.
  107. ^Sola J, Bertschi M, Krauss J (September 2018). "Measuring Pressure: Introducing oBPM, the Optical Revolution for Blood Pressure Monitoring".IEEE Pulse.9(5): 31–33.doi:10.1109/MPUL.2018.2856960.PMID30273141.S2CID52893219.
  108. ^Foti KE, Appel LJ, Matsushita K,Coresh J,Alexander GC, Selvin E (May 2021)."Digit Preference in Office Blood Pressure Measurements, United States 2015-2019".American Journal of Hypertension.34(5): 521–530.doi:10.1093/ajh/hpaa196.PMC8628654.PMID33246327.
  109. ^Prothero JW (2015-10-22).The design of mammals: a scaling approach.Cambridge.ISBN978-1-107-11047-2.OCLC907295832.{{cite book}}:CS1 maint: location missing publisher (link)
  110. ^Brøndum E, Hasenkam JM, Secher NH, Bertelsen MF, Grøndahl C, Petersen KK, et al. (October 2009). "Jugular venous pooling during lowering of the head affects blood pressure of the anesthetized giraffe".American Journal of Physiology. Regulatory, Integrative and Comparative Physiology.297(4): R1058–R1065.doi:10.1152/ajpregu.90804.2008.PMID19657096.
  111. ^Seymour RS, Lillywhite HB (December 1976). "Blood pressure in snakes from different habitats".Nature.264(5587): 664–666.Bibcode:1976Natur.264..664S.doi:10.1038/264664a0.PMID1004612.S2CID555576.
  112. ^Nasoori A, Taghipour A, Shahbazzadeh D, Aminirissehei A, Moghaddam S (September 2014)."Heart place and tail length evaluation in Naja oxiana, Macrovipera lebetina, and Montivipera latifii".Asian Pacific Journal of Tropical Medicine.7S1:S137–S142.doi:10.1016/s1995-7645(14)60220-0.PMID25312108.
  113. ^Seymour RS (1987)."Scaling of cardiovascular physiology in snakes".American Zoologist.27(1): 97–109.doi:10.1093/icb/27.1.97.ISSN0003-1569.
  114. ^abGross DR (2009).Animal Models in Cardiovascular Research(3rd ed.). Dordrecht: Springer. p. 5.ISBN978-0-387-95962-7.OCLC432709394.
  115. ^Brown S, Atkins C, Bagley R, Carr A, Cowgill L, Davidson M, et al. (2007)."Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats".Journal of Veterinary Internal Medicine.21(3): 542–558.doi:10.1111/j.1939-1676.2007.tb03005.x.PMID17552466.
  116. ^Lerman LO, Chade AR, Sica V, Napoli C (September 2005). "Animal models of hypertension: an overview".The Journal of Laboratory and Clinical Medicine.146(3): 160–173.doi:10.1016/j.lab.2005.05.005.PMID16131455.
  117. ^"AKC Canine Health Foundation | Hypertension in Dogs".akcchf.org.Archivedfrom the original on 2022-10-03.Retrieved2022-10-03.
  118. ^Acierno MJ, Brown S, Coleman AE, Jepson RE, Papich M, Stepien RL, Syme HM (November 2018)."ACVIM consensus statement: Guidelines for the identification, evaluation, and management of systemic hypertension in dogs and cats".Journal of Veterinary Internal Medicine.32(6): 1803–1822.doi:10.1111/jvim.15331.PMC6271319.PMID30353952.