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Research Article Free access | 10.1172/JCI106812

Differences in Direct Effects of Adrenergic Stimuli on Coronary, Cutaneous, and Muscular Vessels

Allyn L. Mark, Francois M. Abboud, Phillip G. Schmid, Donald D. Heistad, and Howard E. Mayer

Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and The Veterans Administration Hospital, Iowa City, Iowa 52240

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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and The Veterans Administration Hospital, Iowa City, Iowa 52240

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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and The Veterans Administration Hospital, Iowa City, Iowa 52240

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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and The Veterans Administration Hospital, Iowa City, Iowa 52240

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Cardiovascular Division, Department of Internal Medicine, University of Iowa College of Medicine and The Veterans Administration Hospital, Iowa City, Iowa 52240

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Published February 1, 1972 - More info

Published in Volume 51, Issue 2 on February 1, 1972
J Clin Invest. 1972;51(2):279–287. https://doi.org/10.1172/JCI106812.
© 1972 The American Society for Clinical Investigation
Published February 1, 1972 - Version history
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Abstract

Direct effects of adrenergic stimuli on coronary vessels in dogs were compared with effects on vessels to skin (hind paw) and skeletal muscle (gracilis muscle) after intravenous administration of practolol (2 mg/kg), a selective myocardial beta receptor blocker which minimized indirect effects of myocardial stimulation on coronary vascular resistance. The left circumflex coronary, cranial tibial, and gracilis arteries were perfused separately but simultaneously at constant flow. Perfusion pressures, left ventricular pressure and dP/dt. and heart rate were recorded. Changes in perfusion pressure to each bed reflected changes in vascular resistance.

The direct constrictor effects of sympathetic nerve stimulation, norepinephrine and phenylephrine on coronary vessels were minimal compared with effects on cutaneous and muscular vessels. Subsequent blockade of vascular beta receptors did not augment the constrictor responses. Angiotensin, a nonadrenergic stimulus, produced striking coronary vasoconstriction which exceeded that in skin and approximated that in muscle. These results suggests that there is a paucity of alpha adrenergic receptors in coronary vessels compared to cutaneous and muscular vessels.

Direct dilator responses to isoproterenol were similar in coronary and cutaneous vessels, but were greater in muscular vessels. Responses to glyceryl trinitrate, a nonadrenergic dilator, also were greater in skeletal muscle. Therefore, differences in effects of isoproterenol on the three beds may reflect differences in reactivity to dilator stimuli rather than differences in the density of beta receptors.

In contrast to norepinephrine, the predominant direct effect of epinephrine on coronary vessels was dilatation mediated through activation of vascular beta receptors. A constrictor effect caused by stimulation of alpha receptors was unmasked by propranolol.

Finally, the order of potency of agonists in stimulating coronary vascular beta receptors and the demonstration of selective beta receptor blockade with practolol suggest that beta receptors in coronary vessels resemble those in peripheral vessels more than those in myocardium.

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