Prostaglandin stimulation of renin release: independence of beta-adrenergic receptor activity and possible mechanism of action.

Abstract

Using a continuous superfusion system of rat kidney cortical slices, we investigated the renin-releasing effect of prostaglandin E2 (PGE2) and its possible mechanism of action. PGE2 caused significant stimulation of renin release in a dose-dependent fashion at concentrations of 3 x 10(-6) to 10(-4) M. Isoproterenol (8 x 10(-7) M) stimulated renin release significantly, and its effect was completely abolished by propranolol (2 x 10(-5) M). PGE2-stimulated renin release was not blocked by the same dose of propranolol. Dibutyryl cAMP caused a dose-dependent increase in renin release at concentrations of 10(-5) to 5 x 10(-3) M. Theophylline (4 x 10(-3) M) had no effect on renin release, but when added to subthreshold doses of PGE2 (10(-6) M), it stimulated renin release significantly. The simultaneous addition of maximal stimulating doses of PGE2 and dibutyryl cAMP had no additive or synergistic effects. These experiments show that PGE2 causes stimulation of renin release by a direct effect on the JG cell. The renin-releasing effect of PGE2 does not depend upon the beta-adrenergic receptors but may be mediated through cAMP.