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Journal of Pharmacology And Experimental Therapeutics, Vol. 190, Issue 2, 234-242, 1974
Copyright © 1974 by American Society for Pharmacology and Experimental Therapeutics


AN ANALYSIS OF THE CONTRIBUTION OF THE ENDOCRINE PANCREAS TO THE KALEMOTROPIC ACTIONS OF CATECHOLAMINES

George W. Pettit 1, Robert L. Vick 1, and Charley Roberson 1

1 Department of Physiology, Baylor College of Medicine, Houston, Texas

Constant infusion of epinephrine in the dog causes the concentration of potassium, [K+], in the arterial plasma to increase rapidly, then to decrease to less than the initial value and to continue significantly decreased for the remainder of the infusion. Isoproterenol causes only a fall in plasma [K+]. Recent evidence suggests that decreased release of insulin from the pancreas caused by alpha receptor stimulation and increased release caused by beta receptor stimulation may contribute to the kalemotropic effects of the catecholamines. To test this possibility, we removed the pancreas from dogs anesthetized with morphine-pentobarbital: plasma [K+] increased significantly. Subsequent infusion of epinephrine or isoproterenol (2 µg/kg/min) produced changes in plasma [K+] similar to those obtained in dogs with pancreas intact. These data confirm that the kalemotropic actions of the catecholamines do not depend on release of pancreatic insulin. Slight differences between the pancreatectomized and control groups were attributed to overlapping effects on the intracellular pool of K+ maintained by insulin and that released by alpha receptor agonism and between the intracellular pool of K- maintained by insulin and that increased by beta receptor agonism. Possible contributions to the kalemotropic actions of catecholamines by other endocrinological systems are discussed.

Submitted on September 29, 1973
Accepted on April 5, 1974







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