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Abstract

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 endotheliumderived 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. oa-adrenoceptor activation). 5 The different effects of these therapeutic agents may concur to induce peripheral vasodilatation. Keywords adrenergic neurotransmission bradykinin endothelium-derived contracting factor endothelium-derived relaxing factor prostacyclin shear stress