You are on page 1of 21



Arterial blood pressure
Mean arterial pressure
= Diastolic + 1/3 pulse pressure

Systolic blood pressure

Diastolic blood pressure

Physiological variations in BP

Body mass index.

Determinants of ABP

Total peripheral resistance.

Cardiac output.
Blood viscosity.
Blood volume.

Site of Resistance in the circulation:

?arteries Or capillaries

Total Peripheral Resistance

Factors affecting diameter of

Vasodilator agents:

Atrial natriuretic peptide (ANP)

Nitric oxide

Vasoconstrictor agents:

Sympathomimetic drugs.
Angiotensin II

Blood viscosity: Hematocrit

Blood Viscosity
Plasma Proteins:
Normal Plasma protein level:
Plasma protein


blood viscosity

Effect of Blood Volume :

Changes in blood volume affect arterial pressure by
changing cardiac output:
An increase in blood volume increases
central venous pressure.
right atrial pressure,
right ventricular end-diastolic pressure and volume.
ventricular preload
ventricular stroke volume by the
Frank-Starling mechanism.
right ventricular stroke volume
pulmonary venous
blood flow to the left ventricle, thereby increasing left
ventricular preload and stroke volume.
stroke volume
cardiac output and arterial blood

Regulation of ABP
Short-term regulation:

Baroreceptor reflexes.
Chemoreceptor reflexes.
Atrial reflexes.
CNS-ischemic response.

Long-term regulation:
Role of the kidney.

Intermediate regulation:
Capillary fluid shift

Higher Control of ABP

Of these two sites for arterial baroreceptors, the carotid sinus is
quantitatively the most important for regulating arterial pressure. The
carotid sinus receptors respond to pressures ranging from 60-180
mmHg (Figure 2). Receptors within the aortic arch have a higher
threshold pressure and are less sensitive than the carotid sinus
receptors. Maximal carotid sinus sensitivity occurs near the normal
mean arterial pressure; therefore, very small changes in arterial
pressure around this "set point" dramatically alters receptor firing so
that autonomic control can be reset in such a way that the arterial
pressure remains very near to the set point. This set point changes
during exercise, hypertension, and heart failure. The changing set
point explains how arterial pressure can remain elevated during
. exercise or chronic hypertension

Blood volume regulation by kidneys

Blood volume is determined by the amount of water and sodium

ingested, excreted by the kidneys into the urine, and lost through the
gastrointestinal tract, lungs and skin. The amounts of water and
sodium ingested and lost are highly variable. To maintain blood
volume within a normal range, the kidneys regulate the amount of
water and sodium lost into the urine. For example, if excessive
water and sodium are ingested, the kidneys normally respond by
excreting more water and sodium into the urine. The details of how
the kidneys handle water and sodium are beyond the scope of this
cardiovascular web site; therefore, the reader is encouraged to
consult general medical physiology textbooks to learn more about
this topic. The following paragraphs briefly describe how renal
excretion of water and sodium are regulated and how blood volume
affects cardiovascular function.

Regulation of Blood Volume by Renal

Excretion of Water and Sodium
The primary mechanism by which the kidneys
regulate blood volume is by adjusting the
excretion of water and sodium into the urine.
Pressure Natriuresis:
ed blood volume
arterial pressure, renal
perfusion, and glomerular filtration rate. This leads to
an increase in renal excretion of water and sodium
(Pressure natriuresis).
In certain types of renal disease, the pressure
natriuresis relationship is altered so that the kidneys
retain more sodium and water at a given pressure,
thereby increasing blood volume.

Renin Angiotensin System

The renin-angiotensinaldosterone system
(RAAS) plays an
important role in
regulating blood volume
systemic vascular resista
, which together influence
cardiac output and
arterial pressure.

Functions of Ang II
1. Constricts resistance vessels (via AII [AT1] receptors) thereby

increasing systemic vascular resistance and arterial pressure

2. Acts on the adrenal cortex to release aldosterone, which in
turn acts on the kidneys to increase sodium and fluid retention
3. Stimulates the release of vasopressin )antidiuretic hormone,
ADH) from the posterior pituitary, which increases fluid retention
by the kidneys
4. Stimulates thirst centers within the brain
5. Facilitates norepinephrine release from sympathetic nerve
endings and inhibits norepinephrine re-uptake by nerve endings,
thereby enhancing sympathetic adrenergic function
Stimulates cardiac hypertrophy and vascular hypertrophy