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Journal of Pharmacology And Experimental Therapeutics, Vol. 188, Issue 2, 453-460, 1974
Copyright © 1974 by American Society for Pharmacology and Experimental Therapeutics

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

P. Needleman 1, J. R. Douglas Jr. 1, Barbara Jakschik 1, P. B. Stoecklein 1, and E. M. Johnson Jr. 1

1 Department of Pharmacology, Washington University Medical School, St. Louis, Missouri

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.

Submitted on April 20, 1973
Accepted on October 3, 1973




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Copyright © 1974 by the American Society for Pharmacology and Experimental Therapeutics.