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A Critical Role for Vascular Smooth Muscle in Acute Glucocorticoid-Induced Hypertension

Julie E. Goodwin^*, Junhui Zhang and David S. Geller

Section of Nephrology, Departments of ^* Pediatrics and Medicine, Yale University School of Medicine, New Haven, Connecticut

Correspondence: Dr. David S. Geller, P.O. Box 208029, Section of Nephrology, Yale University School of Medicine, New Haven, CT 06520-8029. Phone: 203-737-5298; Fax: 203-785-4904; E-mail: david.geller{at}yale.edu

Received for publication August 17, 2007. Accepted for publication February 4, 2008.

Although glucocorticoid (GC)-induced hypertension has commonly been attributed to promiscuous activation of the mineralocorticoid receptor by cortisol, thereby promoting excess reabsorption of sodium and water, numerous lines of evidence indicate that this is not the only or perhaps even the primary mechanism. GC induce a number of effects on vascular smooth muscle (VSM) in vitro that may be pertinent to hypertension, but their contribution in vivo is unknown. To address this question, a mouse model with a tissue-specific knockout (KO) of the GC receptor in the VSM was created and characterized. Similar to control mice, KO mice exhibited normal baseline BP and, interestingly, showed normal circadian variation in BP. When dexamethasone was administered, however, the acute hypertensive response was markedly attenuated in KO mice, and there was a trend toward a decreased chronic hypertensive response. These data suggest that the GC receptor in VSM plays a critical role in the acute hypertensive response to GC in vivo.

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				M. Baum and O. W. Moe Glucocorticoid-Mediated Hypertension: Does the Vascular Smooth Muscle Hold All the Answers? J. Am. Soc. Nephrol., July 1, 2008; 19(7): 1251 - 1253. [Full Text] [PDF]

Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673