Info

Angiotensin II

Angiotensinogen, which is synthesized by the liver, is an inactive plasma protein. Renin, a hormone secreted by the granular cells of the juxtaglomer-ular apparatus, promotes the conversion of circulating angiotensinogen into angiotensin I. As angiotensin I travels in the blood through the lungs, it is exposed to the angiotensin-converting enzyme (ACE) located in the endothelial cells lining the blood vessels of the pulmonary circulation. This enzyme converts angiotensin I into angiotensin II.

Angiotensin II has multiple effects throughout the body, all of which directly or indirectly increase MAP. For example, angiotensin II causes the secretion of aldosterone, which enhances sodium reabsorption; expands plasma volume; and increases MAP. Angiotensin II is also a potent vasoactive substance that causes widespread vasoconstriction and therefore an increase in TPR, which increases MAP. Furthermore, angiotensin II causes powerful vasoconstriction in the renal arterioles in particular, which leads to decreased RBF and GFR. Consequently, urine output is reduced and water and solutes are conserved by the body, leading to an increase in plasma volume and therefore MAP. Taken together, these effects demonstrate that the production of angiotensin II is beneficial when blood pressure or blood volume has fallen.

Formation of angiotensin II requires the release of renin from the granular cells. Therefore, the factors affecting renin release must be considered:

• Renal sympathetic nerves

• Intrarenal baroreceptors

• Atrial natriuretic peptide

• Angiotensin II

The sympathetic nervous system increases blood pressure through multiple mechanisms including an increase in cardiac activity and vasoconstriction. Furthermore, stimulation of adrenergic receptors on the granular cells through the activity of renal sympathetic nerves or by circulating epinephrine has a direct stimulatory effect on renin secretion. The enhanced formation of angiotensin II also increases blood pressure through the mechanisms outlined previously. Specifically, angiotensin II constricts the afferent arteriole, decreases RBF, decreases GFR, decreases urine output, and increases plasma volume and blood pressure. Conversely, a decrease in sympathetic activity results in decreased secretion of renin.

The granular cells that secrete renin also serve as intrarenal baroreceptors, monitoring blood volume and blood pressure in the afferent arterioles. Arte-riolar pressure and renin secretion have an inverse relationship; in other words, an increase in blood volume causes an increase in arteriolar blood pressure; increased stimulation of the intrarenal baroreceptors; and decreased secretion of renin. With less angiotensin II-induced vasoconstriction of the afferent arteriole, RBF, GFR, and urine output will increase so that blood volume returns to normal.

The macula densa, which is involved in tubuloglomerular feedback, is also a factor in the regulation of renin secretion. In fact, this mechanism involving the macula densa is thought to be important in the maintenance of arterial blood pressure under conditions of decreased blood volume. For example, a decrease in blood volume leads to a decrease in RBF, GFR, and filtrate flow through the distal tubule. The resulting decrease in the delivery of NaCl to the macula densa stimulates the secretion of renin. Increased formation of angiotensin II serves to increase MAP and maintain blood flow to the tissues.

Atrial natriuretic peptide is released from myocardial cells in the atria of the heart in response to an increase in atrial filling, or an increase in plasma volume. This hormone inhibits the release of renin. With less angiotensin II-induced vasoconstriction of the afferent arteriole, RBF, GFR, and urine output increase. The increased loss of water and solutes decreases blood volume toward normal.

Angiotensin II directly inhibits the secretion of renin from the granular cells. This negative feedback mechanism enables angiotensin II to limit its own formation.

Prostaglandins. The third important factor influencing the resistance of afferent arterioles is the prostaglandins, specifically, PGE2 and PGI2. Produced by the kidney, these prostaglandins function as local vasodilators that decrease arteriole resistance and increase RBF and GFR. Interestingly, the synthesis of PGE2 and PGI2 is stimulated by increased activity of the renal sympathetic nerves and by angiotensin II. The vasodilator prostaglandins then oppose the vasoconstrictor effects of norepinephrine and angiotensin II, resulting in a smaller increase in the resistance of the afferent arterioles. This "dampening" effect is important in that it prevents an excessive reduction in RBF that could lead to renal tissue damage.

Table 19.1 Summary of Factors Affecting Cardiovascular and Renal Systems

Sympathetic nervous activity

T Cardiac output T Total peripheral resistance T Resistance of afferent arteriole —> 4- renal blood flow —> 4- glomerular filtration rate —> 4- Na + filtration

|H,0 filtration

T Renin —> T angiotensin II —> T aldosterone —> T Na+ reabsorption Net effects: 4- urine output; T blood volume; T mean arterial pressure

Angiotensin II

T Total peripheral resistance

T Resistance of afferent arteriole —> 4- renal blood flow —> 4- glomerular filtration rate —> 4- Na + filtration

|H,0 filtration

T Aldosterone —> T Na+ reabsorption T Antidiuretic hormone —> T H20 reabsorption T Thirst T H20 intake

Net effects: 4- urine output; T blood volume; T mean arterial pressure

Atrial natriuretic peptide

4- Renin 4- Aldosterone

4- Total peripheral resistance

Net effects: T urine output; 4- blood volume; 4- mean arterial pressure

Essentials of Human Physiology

Essentials of Human Physiology

This ebook provides an introductory explanation of the workings of the human body, with an effort to draw connections between the body systems and explain their interdependencies. A framework for the book is homeostasis and how the body maintains balance within each system. This is intended as a first introduction to physiology for a college-level course.

Get My Free Ebook


Post a comment