Failure of lndomethacin to Inhibit Saralasin-Stimulated Plasma Renin Activity in Conscious Dogs with Mild Sodium Depletion

Abstract

Abstract

The hypothesis that prostaglandins play a role in the angiotensin II control mechanism for renin release was examined by interrupting the short-loop negative feedback of angiotensin II on the JG cells with the competitive angiotensin II antagonist saralasin. Mildly sodium-depleted conscious dogs received either indomethacin, or the vehicle alone followed by an intravenous infusion of saralasin. Saralasin produced equivalent increases in PRA in the vehicle- and indomethacin-treated groups with no detectable change in arterial pressure. Plasma renin activity increased in the indomethacin-treated group despite a 58% fall in the rate of excretion of PGE₂. These results suggest that in the conscious dog renal prostaglandins do not play an appreciable role in angiotensin II feedback control of renin release.