Renal Vasodilatation After Inhibition of Renin or Converting Enzyme in the Marmoset

Abstract

In both experimental and clinical studies converting enzyme inhibitors have been reported to induce an increase in renal blood flow, which may be important for the chronic antihypertensive efficacy of these agents. A reduction in the renal vasoconstrictor action of angiotensin II (ANG II) may not be the sole mechanism for this increase in renal blood flow. In addition to blocking the conversion of ANG I to ANG II, converting enzyme (kinase II) inhibitors may block the degradation of bradykinin and other peptides (Johnston 1984; Sweet and Blaine 1984). Moreover, the increased concentrations of bradykinin may stimulate renal prostaglandin synthesis (McGiff et al. 1972). Both bradykinin and prostaglandins have been shown to increase renal blood flow after exogenous administration (Gerber et al. 1978; Lonigro et al. 1978). Thus, the renal haemodynamic effects of converting enzyme inhibitors may be mediated by several mechanisms (Clappison et al. 1981; Wong et al. 1981). It has not been possible to clearly elucidate the relative importance of the reduction of ANG II after converting-enzyme inhibition by the use of ANG II antagonists, since these antagonists also possess partial agonist activity (Arendhorst et al. 1977; Zimmerman 1979). The recently developed inhibitors of renin, which specifically block the formation of ANG I, are useful tools for this purpose (Hofbauer and Wood 1984; 1985).