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Independent Effects of Bradykinin on Adenosine 3',5'-Monophosphate and Prostaglandin E₂ Metabolism by Rabbit Renal Medulla^*

Veterans Administration Medical Center, Geriatric Research, Education, and Clinical Center St. Louis, Missouri 63125
Departments of Medicine and Biochemistry, St. Louis University School of Medicine St. Louis, Missouri 63106

Address all correspondence and requests for reprints to: Terry V. Zenser, Ph.D., Veterans Administration Medical Center (111G-JB), St. Louis, Missouri 63125.

Abstract

Bradykinin-stimulated increases in renal prostaglandin (PG) synthesis are thought to result in subsequent increases in cAMP content. This study assesses the relationship between bradykinin-stimulated increases in PGE₂ and cAMP syntheses in renal inner medullary slices. Bradykinin-mediated increases in cAMP (2 min) preceded those in PGE₂ (5 min) synthesis. Forskolin, an activator of adenylate cyclase, increased cAMP, while 2',5'-dideoxyadenosine, an adenylate cyclase inhibitor, reduced cAMP. However, neither agent altered bradykinin-stimulated PGE₂ synthesis. Aspirin decreased basal and abolished bradykinin-stimulated PGE₂ production, but did not alter bradykinin-induced increases in cAMP content. Maximal stimulatory concentrations of 1-methyl-3-isobutylxanthine, a cyclic nucleotide phosphodiesterase inhibitor, and bradykinin were additive in their capacity to increase inner medullary cAMP content. These results suggest that l-methyl-3-isobutylxanthine and bradykinin increase cAMP by separate mechanisms and that bradykinin increases inner medullary cAMP by a direct effect on the production of that cyclic nucleotide. Bradykininmediated increases in cAMP and PGE₂ syntheses by renal medullary slices are independent effects of this renally acting hormone. (Endocrinology 114: 541, 1984)

Footnotes

^* This work was supported by the V.A. and the American Cancer Society, Missouri Division.

Received January 28, 1983.