Central effects of prostaglandin E2 on blood pressure and plasma renin activity in rats. Role of the sympathoadrenal system and vasopressin.

Abstract

This study was designed to determine the roles of the sympathetic nervous system, adrenal medulla, and arginine vasopressin (AVP) in mediating pressor and plasma activity (PRA) responses to intraventricularly (ICV) administered prostaglandin E2 (PGE2) in conscious rats. The ICV PGE2 elevated blood pressure and caused increases in PRA, plasma AVP, and plasma norepinephrine and epinephrine. The pressor effect of ICV PGE2 was not influenced by pretreatment with captopril, but was attenuated by the AVP antagonist, d(CH2)5Tyr(Me)AVP, and by phenoxybenzamine, and was completely abolished by the combination of the AVP antagonist and phenoxybenzamine. The PRA response to ICV PGE2 was not affected by bilateral renal denervation or by phenoxybenzamine alone, but was attenuated by propranolol alone and was completely abolished by the combination of propranolol and phenoxybenzamine. Bilateral adrenomedullectomy did not affect the pressor response to ICV PGE2, whereas it attenuated the increase in PRA and completely abolished the increase in plasma epinephrine. These results suggest that the pressor effect of ICV PGE2 is the result of increased sympathetic nervous system activity and is dependent on the stimulation of alpha-adrenergic receptors and on AVP release. The pressor response to ICV PGE2 is accompanied by but not dependent on an increase in PRA. The renin-stimulating effect of centrally administered PGE2 is, at least in part, dependent on beta-adrenergic receptor stimulation by increased circulating catecholamines.