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- W4205282217 abstract "INVITED REVIEWIntroductionThomas E. LohmeierThomas E. Lohmeier 1 Department of Physiology and Biophysics University of Mississippi Medical Center Jackson, Mississippi 39211 Published Online:01 Nov 1997https://doi.org/10.1152/ajpregu.1997.273.5.R1567MoreSectionsPDF (15 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInEmail The antihypertensive effects of clonidine and related drugs, such as moxonidine and rilmenidine, are believed to be mediated primarily by actions on the central nervous system that inhibit sympathetic outflow. The central actions of clonidine-like agents are generally ascribed to stimulation of medullary α2-adrenergic receptors. However, recent studies have implicated a newly characterized class of imidazoline receptors as playing a role in mediating the sympathoinhibition and hypotension induced by these compounds. Because of the controversial nature of this topic, the following investigators have been asked to express their views on the “role of imidazoline receptors in the central cardiovascular effects of clonidine-like agents.” The first article by Drs. D. J. Reis and J. E. Piletz provides a brief background for this topic. The subsequent articles by Drs. P. Ernsberger and M. Haxhui and by Dr. P. Guyenet express their arguments for and against, respectively, central imidazoline receptor-mediated mechanisms that impact on cardiovascular function.This article has no references to display. Back to Top Next FiguresReferencesRelatedInformation More from this issue > Volume 273Issue 5November 1997Pages R1567-R1568 Copyright & PermissionsCopyright © 1997 the American Physiological Societyhttps://doi.org/10.1152/ajpregu.1997.273.5.R1567PubMed29586561History Published online 1 November 1997 Published in print 1 November 1997 Metrics Downloaded 60 times" @default.
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- W4205282217 title "Introduction" @default.
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