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Description

Quinapril (HCl) is oral angiotensin-converting enzyme (ACE) inhibitor used in the treatment of hypertension and heart failure. Similar to ramipril, quinapril is a prodrug that requires deesterification to the active metabolite quinaprilat. Quinaprilat is threefold more potent than the parent compound. The antihypertensive activity of quinapril is sufficiently long to allow for once-daily dosing. The antihypertensive effects of quinapril are due primarily to a decrease in circulating ACE; the drug does not appear to affect the pressor response to angiotensin II, epinephrine, or norepinephrine. Quinaprilat competes with angiotensin I for angiotensin-converting enzyme, thereby blocking the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor and negative-feedback mediator for renin activity; thus, when quinapril lowers angiotensin II plasma levels, blood pressure decreases and plasma renin activity increases.it inhibits Kininase II (identical to ACE), an enzyme that degrades bradykinin, a potent vasodilator, to inactive peptides, resulting in increased bradykinin levels. Bradykinin-induced vasodilation is thought to be of secondary importance in the blood-pressure lowering effect. A bradykinin mechanism may, however, contribute to ACE-inhibitor-induced angioneurotic edema.

Quinapril (HCl) is oral angiotensin-converting enzyme (ACE) inhibitor used in the treatment of hypertension and heart failure. Similar to ramipril, quinapril is a prodrug that requires deesterification to the active metabolite quinaprilat. Quinaprilat is threefold more potent than the parent compound. The antihypertensive activity of quinapril is sufficiently long to allow for once-daily dosing. The antihypertensive effects of quinapril are due primarily to a decrease in circulating ACE; the drug does not appear to affect the pressor response to angiotensin II, epinephrine, or norepinephrine. Quinaprilat competes with angiotensin I for angiotensin-converting enzyme, thereby blocking the conversion of angiotensin I to angiotensin II. Angiotensin II is a potent vasoconstrictor and negative-feedback mediator for renin activity; thus, when quinapril lowers angiotensin II plasma levels, blood pressure decreases and plasma renin activity increases.it inhibits Kininase II (identical to ACE), an enzyme that degrades bradykinin, a potent vasodilator, to inactive peptides, resulting in increased bradykinin levels. Bradykinin-induced vasodilation is thought to be of secondary importance in the blood-pressure lowering effect. A bradykinin mechanism may, however, contribute to ACE-inhibitor-induced angioneurotic edema.