The Renin AngiotensinAldosterone System Helps Regulate Blood Pressure and Volume

The control of total blood volume is extremely important in regulating arterial pressure. Because changes in total blood volume lead to changes in central blood volume, the long-term influence of blood volume on ventricular end-di-astolic volume and cardiac output is paramount. Cardiac output, in turn, strongly influences arterial pressure. Hormonal control of blood volume depends on hormones that regulate salt and water intake and output as well as red blood cell formation.

Reduced arterial pressure and blood volume cause the release of renin from the kidneys. Renin release is mediated by the sympathetic nervous system and by the direct effect of lowered arterial pressure on the kidneys. Renin is a proteolytic enzyme that catalyzes the conversion of an-giotensinogen, a plasma protein, to angiotensin I (Fig. 18.5). Angiotensin I is then converted to angiotensin II by angiotensin-converting enzyme (ACE), primarily in the lungs. Angiotensin II has the following actions:

• It is a powerful arteriolar vasoconstrictor, and in some circumstances, it is present in plasma in concentrations sufficient to increase SVR.

• It reduces sodium excretion by increasing sodium reabsorption by proximal tubules of the kidney.

• It causes the release of aldosterone from the adrenal cortex.

• It causes the release of AVP from the posterior pituitary gland.

Angiotensin II is a significant vasoconstrictor in some circumstances. Angiotensin II directly stimulates contraction of vascular smooth muscle and also augments NE release from sympathetic nerves and sensitizes vascular smooth muscle to the constrictor effects of NE. It plays an

Angiotensinogen Renin

Angiotensin I

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Essentials of Human Physiology

Essentials of Human Physiology

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