Clonidine antagonizes pressor effect of N-methyl-D-aspartate in the rostral ventrolateral medulla of rats

Lin, J.C.; Liu, D.M.; Wang, Y.

Clinical and Experimental Hypertension 19(7): 1065-1078


ISSN/ISBN: 1064-1963
PMID: 9310204
DOI: 10.3109/10641969709083205
Accession: 008330802

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The purpose of the present study was to investigate the modulatory actions of adrenoreceptor agonists on N-methyl-D-aspartate (NMDA)-induced pressor effect in rostral ventrolateral medulla (RVLM). These drugs were locally applied into RVLM of urethane-anesthetized Sprague-Dawley rats through multibarrel pipettes. Microinjection of NMDA increased the arterial pressure, an effect which was abolished by pretreatment with clonidine, whereas neither the beta-adrenergic agonist isoproterenol nor the alpha-1-adrenergic agonist phenylephrine did alter this pressor response. Previous experiments demonstrated that clonidine binds to noradrenergic alpha-2 and imidazoline receptors in the RVLM. Norepinephrine, which has high affinity for the alpha-2 receptor and low affinity to the imidazoline receptor, partially antagonized NMDA-induced hypertension. On the other hand, administration of selective imidazoline receptor antagonist idazoxan partially reversed clonidine-mediated antagonism of NMDA. Taken together, these results suggest that clonidine may modulate the excitatory amino acid -induced pressor response through noradrenergic alpha-2 and imidazoline receptors in the RVLM.