Am J Physiol Cell Physiol AJP: Gastrointestinal and Liver Physiology
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Am J Physiol Cell Physiol 262: C1284-C1291, 1992;
0363-6143/92 $5.00
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AJP - Cell Physiology, Vol 262, Issue 5 C1284-C1291, Copyright © 1992 by American Physiological Society


ARTICLES

Appearance of alpha 1-adrenergic receptors in soleus muscles from SHR

J. G. Pickar, S. D. Gray and R. C. Carlsen
Department of Human Physiology, University of California, Davis 95616.

The depressed functional capabilities of spontaneously hypertensive rat (SHR) muscles, reported previously (Exp. Neurol. 95: 249-264, 1987), may reflect a decrease in muscle responsiveness to catecholamines occurring as a consequence of exposure to the elevated level of plasma catecholamines in SHR. Responsiveness to applied catecholamines was determined in SHR and Wistar-Kyoto rat (WKY) soleus by measuring muscle resting membrane potentials (RMP) in vitro. Epinephrine (10(-6) M) produced a similar membrane hyperpolarization in SHR and WKY fibers. Pretreatment with the beta-antagonist propranolol completely blocked the epinephrine-induced hyperpolarization in WKY, but not in SHR. SHR soleii from both young and old rats contained a population of alpha 1-adrenergic receptors also associated with membrane hyperpolarization. The alpha-receptors appeared to be associated with a ligand-gated Ca(2+)-influx pathway, since the alpha-agonist-induced membrane hyperpolarization required the presence of Ca2+ in the extracellular medium. The alpha-induced hyperpolarization was also blocked by apamin, a derivative of bee venom which blocks a Ca(2+)-activated K(+)-efflux pathway in a variety of tissues. The possible role of these novel alpha-receptors in skeletal muscle function, and their relationship to the development of hypertension, is uncertain.





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