Catecholamine-induced renin release in the anesthetized mongrel dog is due to both alpha and beta adrenoceptor stimulation: evidence that only the alpha adrenoceptor component is prostaglandin mediated.

The role of renal alpha and beta adrenoceptor activation and prostaglandin synthesis in mediating renin release to intrarenal infusions of the natural neurotransmitters, norepinephrine and epinephrine, was assessed in anesthetized mongrel dogs. Intrarenal infusions of norepinephrine and epinephrine at doses adjusted to reduce renal blood flow by 20 and 50% of baseline values elicited renin release that was not completely blocked by either alpha adrenoceptor blockade with phentolamine or beta adrenoceptor blockade with propranolol. The renin release that persisted during propranolol administration was abolished by the alpha adrenoceptor antagonist, phentolamine, and by the prostaglandin synthetase inhibitor, indomethacin. The beta adrenergic component of renin release, elicited in the presence of phentolamine, was not blocked by indomethacin but abolished by propranolol. These data are consistent with the hypothesis that norepinephrine and epinephrine stimulate renin release by activation of both the renal beta and renal alpha adrenoceptors. The beta adrenoceptor-stimulated renin release appears to be direct and independent of the prostaglandin system, whereas the alpha adrenoceptor-stimulated renin release appears to be indirect and dependent on the generation of endogenous prostaglandins.