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Research Article Free access | 10.1172/JCI106888

Effects of Catecholamines and their Interaction with Other Hormones on Cyclic 3′,5′-Adenosine Monophosphate of the Kidney

Nama P. Beck, Sarah W. Reed, H. V. Murdaugh, and Bernard B. Davis

Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

Medical Service, Veterans Administration Hospital, Pittsburgh, Pennsylvania 15213

Find articles by Beck, N. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

Medical Service, Veterans Administration Hospital, Pittsburgh, Pennsylvania 15213

Find articles by Reed, S. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

Medical Service, Veterans Administration Hospital, Pittsburgh, Pennsylvania 15213

Find articles by Murdaugh, H. in: JCI | PubMed | Google Scholar

Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

Medical Service, Veterans Administration Hospital, Pittsburgh, Pennsylvania 15213

Find articles by Davis, B. in: JCI | PubMed | Google Scholar

Published April 1, 1972 - More info

Published in Volume 51, Issue 4 on April 1, 1972
J Clin Invest. 1972;51(4):939–944. https://doi.org/10.1172/JCI106888.
© 1972 The American Society for Clinical Investigation
Published April 1, 1972 - Version history
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Abstract

Catecholamines have several physiological effects on the kidney. These include: (a) stimulation of renin synthesis in the cortex: (b) antidiuresis by beta adrenergic agents; and (c) diuresis by alpha adrenergic stimulation. The role of cyclic 3′,5′-adenosine monophosphate (cyclic AMP) in the renal actions of catecholamines was evaluated by measuring the effects of several adrenergic agents on cyclic AMP concentration in the dog kidney.

Beta adrenergic activity increased cyclic AMP concentration in the renal cortex, a finding consistent with the hypothesis that beta-adrenergic stimulation augments renin synthesis by increasing cyclic AMP generation.

Beta adrenergic stimulation, like vasopressin, increased cyclic AMP concentration in the renal medulla. This suggests that beta adrenergic stimulation causes antidiuresis by augmenting cyclic AMP generation in the renal medulla.

Alpha adrenergic activity inhibited the effect of vasopressin to stimulate cyclic AMP generation. These results support the hypothesis that the diuretic effect of alpha adrenergic stimulation is mediated by inhibition of the effect of vasopressin to increase cyclic AMP generation.

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