Afferent arteriolar dilation stimulates renin release via increased prostaglandin synthesis, whereas isoproterenol stimulates renin release independently of prostaglandins.
Does not support clinical translation yet; extends animal evidence for prostaglandin-dependent versus independent renin pathways.
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.
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VIKSE et al. (1984) studied this question.
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