Hypertension, Vol 4, 809-816, Copyright © 1982 by American Heart Association
T Okuno, MD Lindheimer and S Oparil
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.
ARTICLES
Central effects of prostaglandin E2 on blood pressure and plasma renin activity in rats. Role of the sympathoadrenal system and vasopressin
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