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Free access | 10.1172/JCI109304

Dopamine during α- or β-Adrenergic Blockade in Man: HORMONAL, METABOLIC, AND CARDIOVASCULAR EFFECTS

Mara Lorenzi, John H. Karam, Eva Tsalikian, Nancy V. Bohannon, John E. Gerich, and Peter H. Forsham

Metabolic Research Unit and Department of Medicine, University of California, San Francisco, San Francisco, California 94143

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Metabolic Research Unit and Department of Medicine, University of California, San Francisco, San Francisco, California 94143

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Metabolic Research Unit and Department of Medicine, University of California, San Francisco, San Francisco, California 94143

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Metabolic Research Unit and Department of Medicine, University of California, San Francisco, San Francisco, California 94143

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Metabolic Research Unit and Department of Medicine, University of California, San Francisco, San Francisco, California 94143

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Metabolic Research Unit and Department of Medicine, University of California, San Francisco, San Francisco, California 94143

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Published February 1, 1979 - More info

Published in Volume 63, Issue 2 on February 1, 1979
J Clin Invest. 1979;63(2):310–317. https://doi.org/10.1172/JCI109304.
© 1979 The American Society for Clinical Investigation
Published February 1, 1979 - Version history
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Abstract

We studied the contribution of α- and β-adrenergic receptor activation to the cardiovascular, metabolic, and hormonal effects of dopamine. At a concentration of 1.5 μg/kg·min, the infusion of dopamine in 12 normal volunteers was associated with a transient but significant rise in pulse rate, which was prevented by propranolol. Venous plasma glucose did not change throughout the experiments, and a mild increase in plasma free fatty acid levels observed during the administration of dopamine alone was antagonized by propranolol. In contrast, neither the β-adrenergic blocker, propranolol, nor the α-adrenergic blocker, phentolamine, was effective in inhibiting the dopamine-induced rise in plasma glucagon (from 82±9 to 128±14 pg/ml; P < 0.005) and serum insulin (from 7.5±1 to 13±1.5 μU/ml; P < 0.005) or its suppression of plasma prolactin (from 8.5±1 to 5.2±0.8 ng/ml; P < 0.001). Although serum growth hormone levels did not change during the infusion of dopamine alone, an obvious rise occurred in three subjects during the combined infusion of propranolol and dopamine.

Whereas some metabolic and cardiovascular effects of dopamine are mediated through adrenergic mechanisms, these observations indicate that this is not the case for the effects of this catecholamine on glucagon, insulin, and prolactin secretion, and thus provide further support for the theory of a specific dopaminergic sensitivity of these hormonal systems in man.

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