Since their introduction in 1980, angiotensin-converting enzyme (ACE) inhibitors, because of their unique pharmacologic properties, have proven superior to other vasodilators in the management of heart failure and have come to play a key role in the therapy of hypertension. They are particularly useful in hypertensive patients with diabetes and proteinuria.
A. Mechanism of Action
The sodium concentration in the distal kidney tubules, sensed by the macula densa, controls the release of renin from the specialized juxtaglomerular cells located in the media of the afferent kidney arterioles. Renin is an enzyme that profoundly affects the cardiovascular system. It is a protease that cleaves the leucine 10–valine 11 bond from the circulating precursor angiotensinogen to form the decapep-tide angiotensin I. ACE in the lungs cleaves histidine-leucine from angiotensin I, resulting in the formation of angiotensin II, which produces the effects listed below.
1. Vasoconstriction that is more intense than that caused by norepinephrine. This vasoconstriction occurs mainly in arterioles and, to a small degree, in veins. This action is more pronounced in skin and in the kidney but with some sparing of vessels in the brain and muscle.

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