Experimental Physiology
	

Celebrating 100 years
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Physiology in Press

First published online on June 15, 2007.
Experimental Physiology (2007)
DOI: 10.1113/expphysiol.2007.037861
© The Physiological Society 2007

A more recent version of this article appeared on September 1, 2007
This Article
Right arrow Full Text (Rapid PDF)
Right arrow All Versions of this Article:
92/5/849    most recent
expphysiol.2007.037861v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Wang, L.-G.
Right arrow Articles by Wang, W.-Z.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Wang, L.-G.
Right arrow Articles by Wang, W.-Z.

Received March 15, 2007
Revised April 13, 2007
Accepted after revision June 11, 2007


Cardiovascular Control [210]

Comparative study of NMDA and AMPA/kainate receptors involved in cardiovascular inhibition of imidazoline-like drugs

Li-Gang Wang 1, Jun Zeng 2, Wen-Jun Yuan 1, Ding-Feng Su 1, Wei-Zhong Wang 1*

1 Second Military Medical University
2 Zhongshan Hospital

* To whom correspondence should be addressed. E-mail: wangwz68{at}hotmail.com.


   Abstract
The depressor mechanism of imidazoline-like drugs is believed to result from activation of I1-imidazoline receptors (I1R) and/or {alpha}2-adrenoceptors ({alpha}2AR) within the central nervous system, which is associated with the glutamatergic system. The rostral ventrolateral medulla (RVLM) has been recognized as a specific target area mediating depressor action of imidazoline-like drugs. The objective of this study was to comparatively determine the effects of blockade of the central glutamate receptor subtypes N-methyl-D-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methyl-4- isoxazolepropionic acid (AMPA)/kainate on the cardiovascular effects of imidazoline-like drugs (clonidine and moxonidine) in anesthetized rats. Intracerebroventricular (ICV) injection of the NMDA receptor antagonist MK801 or the AMPA/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) produced similar reductions in decreased blood pressure (BP) and heart rate (HR) induced by ICV injection of clonidine. ICV injection of the glutamate receptor antagonist kynurenic acid not only abolished clonidine-induced hypotension and bradycardia but also converted the responses to a pressor action and tachycardia. Unilateral RVLM injection of MK801 or CNQX significantly attenuated intra-RVLM clonidine-induced decreases in BP and HR. We further found that unilateral injection of a selective I1R agonist moxonidine significantly decreased BP and HR, which is also remarkably attenuated to a similar extent by prior injection of MK801 or CNQX. In conclusion, these data show that blockade of central (RVLM) NMDA and AMPA/kainate receptors exhibits a similar importance in attenuating the decreased BP and HR induced by clonidine or moxonidine. It is suggested that both NMDA and AMPA/kainate receptors are involved in the cardiovascular inhibition of imidazoline-like drugs, which probably is, at least partially, dependent on an I1R mechanism in the RVLM.

Key Words: Blood pressure, Cardiovascular, Rostral ventrolateral medulla







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2007 by the The Physiological Society.