Relationship between PGE₂ and renin release in dog kidneys Effects of afferent arteriolar dilation and adrenergic stimulation

Abstract

To study the relationship between PGE2 and renin release from the kidney, examinations were performed on anesthetized dogs during afferent arteriolar dilation. This condition is known to increase renin release and enhance the stimulatory effects on renin release of beta-adrenergic agonists, such as isoproterenol. Afferent arteriolar dilation induced by constricting the renal artery or occluding the ureter increased PGE2 and renin release before, but not after, indomethacin administration. Isoproterenol infusion during afferent arteriolar dilation increased renin release but not PGE2 release both before and after indomethacin administration. Phenylephrine, an alpha-adrenergic agonist, which also induces afferent arteriolar dilation, increased PGE2 and renin release at control blood pressure but not when the afferent arterioles already were dilated by ureteral occlusion. We conclude that afferent arteriolar dilation caused by renal arterial constriction, ureteral occlusion or infusion of phenylephrine increases prostaglandin synthesis which stimulates renin release. The effect of isoproterenol on renin release is independent of prostaglandin synthesis.

Properties of the macula densa mechanism for renin release in the dog

“…Prostaglandins. Although other stimulators of renin release exist, most if not all the renin release induced by lowering RAP or occluding the ureter is probably due to intrarenal stimulation of prostaglandin synthesis in the absence of sympathetic stimulation (Data et al 1978, Vikse et al 1984. Autoregulatory vasodilation both increases pre-glomerular synthesis of prostaglandins and enhances the stimulatory effect of prostaglandins on renin release .…”

Stimulation of renin release by PGE2 and PGI2 infusion in the dog: enhancing effect of ureteral occlusion or administration of ethacrynic acid

“…of prostaglandin synthesis almost abolishes the renin relase induced by activation of these mechanisms (Data et al 1978, Gerber et al 1981, Vikse et al 1984, Bugge et al 1988a. A main part of buih PGE, and PGI, synthesis seems to take place in the preglomerular vascular tree (Vikse et al 1985, Bugge et al 1987), and both prostaglandins are released during reduction in renal arterial pressure (RAP) or elevation of ureteral pressure (Jackson et al 1982, , Bugge et al 1986.…”