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Am J Physiol Regul Integr Comp Physiol 273: R1567-R1568, 1997;
0363-6119/97 $5.00
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Vol. 273, Issue 5, R1567-R1568, November 1997

INVITED REVIEW

Thomas E. Lohmeier

Department of Physiology and Biophysics University of Mississippi Medical Center Jackson, Mississippi 39211 

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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 alpha 2-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.

AJP Regul Integr Compar Physiol 273(5):R1567-R1568



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