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Cardiovascular and antidiuretic effects of central prostaglandin E2.
Author(s) -
Hoffman W E,
Schmid P G
Publication year - 1979
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1979.sp012688
Subject(s) - antidiuretic , medicine , endocrinology , phenoxybenzamine , blood pressure , prostaglandin e2 , heart rate , tachycardia , prostaglandin , hormone , chemistry , receptor
1. Unanaesthetized normal and water‐loaded rats were tested for cardiovascular and antidiuretic responses to intracerebroventricular (I.V.T.) injections of prostaglandin E2 (PGE2). 2. I.V.T. injections of PGE2 produced tachycardia and a slow rise in blood pressure that reached a peak in 15 min and lasted up to 2 hr. 3. Intravenous pre‐treatment with phenoxybenzamine, an alpha‐adrenergic blocker, inhibited pressor but not heart rate responses to I.V.T. PGE2. Pre‐treatment with propranalol, a beta‐adrenergic blocker, inhibited tachycarcia but not pressor responses to I.V.T. PGE2. Atropine attenuated heart rate and blood pressure responses when higher doses of PGE2 were tested. 4. In water‐loaded rats, I.V.T. PGE2 produced antidiuretic effects suggesting release of antidiuretic hormone in subpressor amounts. Antidiuretic but not cardiovascular responses to I.V.T. PGE2 were abolished by median eminence lesions. 5. Intravenous PGE2 infusions produced a decrease in blood pressure and no antidiuretic effects, indicating that both responses were centrally mediated. 6. The results indicate that I.V.T. PGE2 produces pressor and tachycardia responses in the unanaesthetized rat which are mediated primarily by centrally mediated sympathetic outflow.