Lack of effect of captopril on preglomerular renal microvascular prostanoid biosynthesis.

Extensive research has focused on the mechanisms by which converting enzyme inhibitors, such as captopril, lower the systemic blood pressure. In addition to inhibiting the conversion of angiotensin I to angiotensin II, these agents have been proposed to influence other systems which might affect vascular resistance including the kinins and the prostanoids. This study was designed to evaluate whether captopril has any direct effect to increase the synthesis of endogenous vasodilator prostanoids in either freshly isolated rabbit renal preglomerular microvessels or in endothelial cells derived from them. The results indicate that captopril, in a variety of doses, had no effect on the synthesis of either prostacyclin or PGE2 by renal preglomerular microvessels. Bradykinin, on the other hand, increased prostanoid production significantly in the same tissue preparations. Finally, captopril had no effect in altering bradykinin-induced increases in renovascular prostanoid biosynthesis. Thus, captopril appears to have no ability to enhance the production of vasodilator prostanoids in rabbit renal preglomerular resistance vessels. These data question the role of prostanoid-related mechanisms in the non-renin-related antihypertensive actions of captopril.