ACEs participate in the renin-angiotensin-aldosterone system to have which of the following physiologic effects?
A. Inhibit conversion of angiotensin II to angiotensin I.
B. Vasoconstriction and sodium depletion.
C. Promote sodium and water retention.
D. Stimulate vasodilation and inhibit sodium depletion.
Correct Answer: C. Promote sodium and water retention.
Angiotensin is a potent vasoconstrictor that stimulates the release of aldosterone. Aldosterone release promotes sodium and water retention. The renin–angiotensin–aldosterone system (RAAS) is a critical regulator of blood volume and systemic vascular resistance. While the baroreceptor reflex responds in a short-term manner to decreased arterial pressure, the RAAS is responsible for more chronic alterations. It is composed of three major compounds: renin, angiotensin II, and aldosterone.
Option A: The conversion of angiotensin I to II is not inhibited. The conversion of angiotensin I to angiotensin II is catalyzed by an enzyme called angiotensin-converting enzyme (ACE). ACE is found primarily in the vascular endothelium of the lungs and kidneys. After angiotensin I is converted to angiotensin II, it has effects on the kidney, adrenal cortex, arterioles, and brain by binding to angiotensin II type I (AT) and type II (AT) receptors.
Option B: Aldosterone promotes sodium retention, not depletion. Aldosterone is a steroid hormone that causes an increase in sodium reabsorption and potassium excretion at the distal tubule and collecting duct of the nephron. Aldosterone works by stimulating the insertion of luminal Na channels and basolateral Na-K ATPase proteins. The net effect is an increased level of sodium reabsorption.
Option D: The effect of angiotensin II on vasoconstriction takes place in systemic arterioles. Here, angiotensin II binds to G protein-coupled receptors, leading to a secondary messenger cascade that results in potent arteriolar vasoconstriction. This acts to increase total peripheral resistance, causing an increase in blood pressure.