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Comparative study of NMDA and AMPA/kainate receptors involved in cardiovascular inhibition produced by imidazoline-like drugs in anaesthetized rats.
Exp Physiol. 2007 Sep; 92(5):849-58.EP

Abstract

The depressor mechanism of imidazoline-like drugs is believed to result from activation of I(1)-imidazoline receptors (I(1)R) and/or alpha(2)-adrenoceptors within the central nervous system, which are associated with the glutamatergic system. The rostral ventrolateral medulla (RVLM) has been recognized as a specific target area that mediates the depressor action of imidazoline-like drugs. The objective of this study was to determine the comparative effects of blockade of the central glutamate receptor subtypes N-methyl-d-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate on the cardiovascular actions of imidazoline-like drugs (clonidine and moxonidine) in anaesthetized rats. Intracerebroventricular (i.c.v.) 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 blood pressure (BP) and heart rate (HR) to those induced by I.C.V. injection of clonidine. Intracerebroventricular injection of the glutamate receptor antagonist kynurenic acid not only abolished clonidine-induced hypotension and bradycardia but converted the responses to a pressor action and tachycardia. Unilateral injection of MK801 or CNQX into RVLM significantly attenuated intra-RVLM clonidine-induced decreases in BP and HR. We also found that unilateral injection of a selective I(1)R agonist, moxonidine, significantly decreased BP and HR, which were also 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 produces similar attenuation of the decrease in BP and HR induced by clonidine or moxonidine. It is suggested that both NMDA and AMPA/kainate receptors are involved in the cardiovascular inhibition produced by imidazoline-like drugs, which is probably at least partly dependent on an I(1)R mechanism in the RVLM.

Authors+Show Affiliations

Department of Physiology, Second Military Medical University, 800 Xiang-Yin Road, Shanghai 200433, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17573415

Citation

Wang, Li-Gang, et al. "Comparative Study of NMDA and AMPA/kainate Receptors Involved in Cardiovascular Inhibition Produced By Imidazoline-like Drugs in Anaesthetized Rats." Experimental Physiology, vol. 92, no. 5, 2007, pp. 849-58.
Wang LG, Zeng J, Yuan WJ, et al. Comparative study of NMDA and AMPA/kainate receptors involved in cardiovascular inhibition produced by imidazoline-like drugs in anaesthetized rats. Exp Physiol. 2007;92(5):849-58.
Wang, L. G., Zeng, J., Yuan, W. J., Su, D. F., & Wang, W. Z. (2007). Comparative study of NMDA and AMPA/kainate receptors involved in cardiovascular inhibition produced by imidazoline-like drugs in anaesthetized rats. Experimental Physiology, 92(5), 849-58.
Wang LG, et al. Comparative Study of NMDA and AMPA/kainate Receptors Involved in Cardiovascular Inhibition Produced By Imidazoline-like Drugs in Anaesthetized Rats. Exp Physiol. 2007;92(5):849-58. PubMed PMID: 17573415.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Comparative study of NMDA and AMPA/kainate receptors involved in cardiovascular inhibition produced by imidazoline-like drugs in anaesthetized rats. AU - Wang,Li-Gang, AU - Zeng,Jun, AU - Yuan,Wen-Jun, AU - Su,Ding-Feng, AU - Wang,Wei-Zhong, Y1 - 2007/06/15/ PY - 2007/6/19/pubmed PY - 2007/10/30/medline PY - 2007/6/19/entrez SP - 849 EP - 58 JF - Experimental physiology JO - Exp Physiol VL - 92 IS - 5 N2 - The depressor mechanism of imidazoline-like drugs is believed to result from activation of I(1)-imidazoline receptors (I(1)R) and/or alpha(2)-adrenoceptors within the central nervous system, which are associated with the glutamatergic system. The rostral ventrolateral medulla (RVLM) has been recognized as a specific target area that mediates the depressor action of imidazoline-like drugs. The objective of this study was to determine the comparative effects of blockade of the central glutamate receptor subtypes N-methyl-d-aspartate (NMDA) or alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)/kainate on the cardiovascular actions of imidazoline-like drugs (clonidine and moxonidine) in anaesthetized rats. Intracerebroventricular (i.c.v.) 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 blood pressure (BP) and heart rate (HR) to those induced by I.C.V. injection of clonidine. Intracerebroventricular injection of the glutamate receptor antagonist kynurenic acid not only abolished clonidine-induced hypotension and bradycardia but converted the responses to a pressor action and tachycardia. Unilateral injection of MK801 or CNQX into RVLM significantly attenuated intra-RVLM clonidine-induced decreases in BP and HR. We also found that unilateral injection of a selective I(1)R agonist, moxonidine, significantly decreased BP and HR, which were also 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 produces similar attenuation of the decrease in BP and HR induced by clonidine or moxonidine. It is suggested that both NMDA and AMPA/kainate receptors are involved in the cardiovascular inhibition produced by imidazoline-like drugs, which is probably at least partly dependent on an I(1)R mechanism in the RVLM. SN - 0958-0670 UR - https://www.unboundmedicine.com/medline/citation/17573415/Comparative_study_of_NMDA_and_AMPA/kainate_receptors_involved_in_cardiovascular_inhibition_produced_by_imidazoline_like_drugs_in_anaesthetized_rats_ L2 - https://doi.org/10.1113/expphysiol.2007.037861 DB - PRIME DP - Unbound Medicine ER -