Why are converting enzyme inhibitors vasodilators?

• Published in: British journal of clinical pharmacology Vol. 28; no. S2; pp. 95S - 104S
• Main Authors: Vanhoutte, PM, Auch‐Schwelk, W, Biondi, ML, Lorenz, RR, Schini, VB, Vidal, MJ
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 1989; Blackwell Science
• Subjects: Angiotensin-Converting Enzyme Inhibitors - pharmacology; Animals; Biological and medical sciences; Cardiovascular system; Medical sciences; Pharmacology. Drug treatments; Vasodilator Agents - pharmacology; Vasodilator agents. Cerebral vasodilators; Vasomotricity; Vasodilator agent; Angiotensin converting enzyme; Enzyme inhibitor; Adrenergic transmission; Mechanism of action; Endothelium
• ISSN: 0306-5251; 1365-2125
• DOI: 10.1111/j.1365-2125.1989.tb03585.x

1. The primary action of the converting enzyme inhibitors to prevent the formation of angiotensin II can explain a decrease in peripheral vascular resistance in patients with elevated, but not in those with normal or reduced plasma renin levels. 2. The inhibition of the breakdown of bradykinin will potentiate the vasodilator properties of the endogenously produced peptide. These include direct relaxation of certain vascular smooth muscle, production of vasodilator prostanoids and release of endothelium‐derived relaxing factor(s). The greater release of the latter in the kidney could exert a negative feedback on the release of renin. 3. In addition, converting enzyme inhibitors may directly (by a prejunctional effect) and indirectly (by curtailing the production of angiotensin II) reduce the release of noradrenaline in the blood vessel wall. 4. Converting enzyme inhibitors may also directly reduce the responsiveness of vascular smooth muscle to vasoconstrictor stimuli (e.g. alpha‐adrenoceptor activation). 5. The different effects of these therapeutic agents may concur to induce peripheral vasodilatation.