Figure 199

Renin-angiotensin vasoconstrictor mechanism for arterial pressure control.

arterioles immediately proximal to the glomeruli. When the arterial pressure falls, intrinsic reactions in the kidneys themselves cause many of the prorenin molecules in the JG cells to split and release renin. Most of the renin enters the renal blood and then passes out of the kidneys to circulate throughout the entire body. However, small amounts of the renin do remain in the local fluids of the kidney and initiate several intrarenal functions.

Renin itself is an enzyme, not a vasoactive substance. As shown in the schema of Figure 19-9, renin acts enzymatically on another plasma protein, a globulin called renin substrate (or angiotensinogen), to release a 10-amino acid peptide, angiotensin I. Angiotensin I has mild vasoconstrictor properties but not enough to cause significant changes in circulatory function. The renin persists in the blood for 30 minutes to 1 hour and continues to cause formation of still more angiotensin I during this entire time.

Within a few seconds to minutes after formation of angiotensin I, two additional amino acids are split from the angiotensin I to form the 8-amino acid peptide angiotensin II. This conversion occurs almost entirely in the lungs while the blood flows through the small vessels of the lungs, catalyzed by an enzyme called converting enzyme that is present in the endothelium of the lung vessels.

Angiotensin II is an extremely powerful vasoconstrictor, and it also affects circulatory function in other ways as well. However, it persists in the blood only for 1 or 2 minutes because it is rapidly inactivated by multiple blood and tissue enzymes collectively called angiotensinases.

During its persistence in the blood, angiotensin II has two principal effects that can elevate arterial pressure. The first of these, vasoconstriction in many areas of the body, occurs rapidly. Vasoconstriction occurs intensely in the arterioles and much less so in the veins. Constriction of the arterioles increases the total peripheral resistance, thereby raising the arterial pressure, as demonstrated at the bottom of the schema in Figure 19-9. Also, the mild constriction of the veins promotes increased venous return of blood to the heart, thereby helping the heart pump against the increasing pressure.

The second principal means by which angiotensin increases the arterial pressure is to decrease excretion of both salt and water by the kidneys. This slowly increases the extracellular fluid volume, which then increases the arterial pressure during subsequent hours and days. This long-term effect, acting through the extracellular fluid volume mechanism, is even more powerful than the acute vasoconstrictor mechanism in eventually raising the arterial pressure.

Rapidity and Intensity of the Vasoconstrictor Pressure Response to the Renin-Angiotensin System

Figure 19-10 shows a typical experiment demonstrating the effect of hemorrhage on the arterial pressure under two separate conditions: (1) with the renin-angiotensin system functioning and (2) without

Figure 19-10

Pressure-compensating effect of the renin-angiotensin vasoconstrictor system after severe hemorrhage. (Drawn from experiments by Dr. Royce Brough.)

the system functioning (the system was interrupted by a renin-blocking antibody). Note that after hemorrhage—enough to cause acute decrease of the arterial pressure to 50mmHg—the arterial pressure rose back to 83 mm Hg when the renin-angiotensin system was functional. Conversely, it rose to only 60mmHg when the renin-angiotensin system was blocked. This shows that the renin-angiotensin system is powerful enough to return the arterial pressure at least halfway back to normal within a few minutes after severe hemorrhage. Therefore, sometimes it can be of lifesaving service to the body, especially in circulatory shock.

Note also that the renin-angiotensin vasoconstrictor system requires about 20 minutes to become fully active. Therefore, it is somewhat slower to act for pressure control than are the nervous reflexes and the sympathetic norepinephrine-epinephrine system.

Effect of Angiotensin in the Kidneys to Cause Renal Retention of Salt and Water— An Especially Important Means for Long-Term Control of Arterial Pressure

Angiotensin causes the kidneys to retain both salt and water in two major ways:

1. Angiotensin acts directly on the kidneys to cause salt and water retention.

2. Angiotensin causes the adrenal glands to secrete aldosterone, and the aldosterone in turn increases salt and water reabsorption by the kidney tubules.

Thus, whenever excess amounts of angiotensin circulate in the blood, the entire long-term renal-body fluid mechanism for arterial pressure control automatically becomes set to a higher arterial pressure level than normal.

Angiotensin levels in the blood

Angiotensin levels in the blood

Arterial pressure (mm Hg)

Figure 19-11

Arterial pressure (mm Hg)

Figure 19-11

Mechanisms of the Direct Renal Effects of Angiotensin to Cause Renal Retention of Salt and Water. Angiotensin has several direct renal effects that make the kidneys retain salt and water. One major effect is to constrict the renal arterioles, thereby diminishing blood flow through the kidneys. As a result, less fluid filters through the glomeruli into the tubules. Also, the slow flow of blood reduces the pressure in the peritubular capillaries, which causes rapid reabsorption of fluid from the tubules. And still a third effect is that angiotensin has important direct actions on the tubular cells themselves to increase tubular reabsorption of sodium and water. The total result of all these effects is significant, sometimes decreasing urine output less than one fifth of normal.

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