The central α-adrenoceptor role in cardiovascular responses to intracerebroventricular (i.c.v.) injection of neostigmine, a tertiary anticholinesterase, was studied in conscious sham-operated and sinoaortic-denervated rats. Neostigmine (0.1-1 μg i.c.v.) showed dose-dependent pressor and bradycardiac effects in vehicle-pretreated sham-operated rats but only an increased pressor effect in sinoaortic-denervated animals. The pretreatment with the catecholaminergic neurotoxin, 6-hydroxydopamine (250 μg i.c.v.), given 72 h previous to the corresponding operation, blunted the cardiovascular effects of neostigmine in both groups of rats. Prazosin (10 and 30 μg i.c.v.), an α1-adrenoceptor antagonist, prevented the pressor response to neostigmine (0.3 μg i.c.v.) in sham-operated and sinoaortic-denervated rats. Yohimbine, an α2-adrenoceptor antagonist (10 and 30 μg i.c.v.), only prevented the bradycardia induced by neostigmine (0.3 μg i.c.v.) in the sham-operated rats. 6-Hydroxydopamine pretreatment lowered the norepinephrine content in hypothalamus, midbrain, medulla oblongata and spinal cord, but did not modify it in the pons, in sham-operated rats and sinoaortic-denervated animals. The present results suggested that brain α1-adrenoceptors would mediate the pressor response to neostigmine (i.c.v.) in sham-operated and sinoaortic-denervated rats and central α2-adrenoceptors mediate the bradycardia in sham-operated rats. This work lends support to the view that cardiovascular responses to brain cholinergic stimulation in sham-operated and sinoaortic-denervated rats could be mediated by a central catecholaminergic activation. © 1994.
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