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pubmed:abstractText |
3-Mercaptopropionic acid (3-MP), an inhibitor of the synthesis of GABA, acts in the central nervous system to increase arterial pressure (+50-60 mmHg) in anesthetized guinea pigs, apparently by sympathoadrenal activation. However, blockade of nicotinic receptors in autonomic ganglia with hexamethonium (10 or 20 mg/kg, i.v.) failed to effect any degree of sustained reversal of increases in blood pressure. Infusion of atropine methyl bromide (1 mg/kg, i.v.) likewise was without effect when administered alone, but completely reversed the hypertension induced by 3-MP when given after treatment with hexamethonium. These findings suggest that ganglionic transmission through either the "classical" nicotinic pathway or a muscarinic pathway is sufficient to sustain the sympathetically-mediated pressor response elicited by 3-MP.
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