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Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blocker
Questions
1
Describe the mechanism of action of antiogensin-converting enzyme inhibitors and angiotensin receptor blockers?
The renin-angiotensin-aldosterone system plays an essential role in the maintenance of blood pressure, and hence drugs that target this system are effective antihypertensive agents. In this system, the substrate, angiotensinogen, is cleaved by renin to generate angiotensin-I. Angiotensin-converting enzyme (ACE) converts angiotensin-I to angiotensin-II which then increases blood pressure through effects on angiotensin type 1 receptor by mediating vasoconstriction, sodium reabsorption in the renal tubule, stimulating aldosterone synthesis, and activating the sympathetic nervous system. ACE inhibitors competitively inhibit the conversion of angiotensin-I to angiotensin-II, whereas angiotensin receptor blockers (ARBs) prevent binding of angiotensin-II to angiotensin type 1 receptor ( Fig. 31.1 ). In contrast to the effect on angiotensin type 1 receptor, binding of angiotensin-II to angiotensin type 2 receptor causes vasodilation and sodium excretion.
2
What differences are seen with regard to the renin-angiotensin-aldosterone system with ACE inhibitors and ARBs? How is it clinically important?
Both ACE inhibitors and ARBs increase plasma levels of renin and angiotensin-I. ARBs increase plasma angiotensin-II levels, whereas ACE inhibitors decrease plasma angiotensin-II levels. Hence, ACE inhibitors reduce the effect on angiotensin type 1 and 2 receptors. ACE inhibitors also prevent degradation of bradykinin, leading to increased kinin levels, which may be responsible for the cough commonly seen in patients taking ACE inhibitors but not ARBs.
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