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RELEASE OF RENAL PROSTAGLANDIN BY CATECHOLAMINES: RELATIONSHIP TO RENAL ENDOCRINE FUNCTION

1974; American Society for Pharmacology and Experimental Therapeutics; Volume: 188; Issue: 2 Linguagem: Inglês

10.1016/s0022-3565(25)29770-1

1521-0103

Philip Needleman, J. R. Douglas, Barbara A. Jakschik, P.B. Stoecklein, Eddie Johnson,

Inflammatory mediators and NSAID effects

Epinephrine and norepinephrine caused vasoconstriction and prostaglandin (PG) release when administered to the isolated perfused rabbit kidney. Dopamine was only about 0.1% as potent as epinephrine as a PG releaser, and isoproterenol did not cause renal PG release. Catecholamine-induced PG release thus appears to be mediated by alpha adrenergic receptor site stimulation, and this was confirmed by the finding that blockade was achieved with phenoxybenzamine but not propranolol. Phenoxybenzarnine did not block PG release induced by angiotensin II, but indomethacin (PG synthesis inhibitor) blocked all PG release. Renal nerve stimulation caused the rabbit kidney to release PG, and this release was blocked by phenoxybenzamine or indomethacin. Paradoxically, tyramine did not cause PG release. Renal ischemia caused PG release which was blocked by indomethacin but was not blocked by phenoxybenzamine and/or propranolol.