Abstract

In chloralose-urethane-anesthetized cats, intravertebral injection of clonidine (0.5–4.0 μ/kg) elicited a drastic suppression of the bradycardia induced by stimulating the gigantocellular reticular nucleus (GRN). The degree of blockage of GRN-induced cardioinhibition was related to the time course of the inherent cardiovascular effects of clonidine. It was also dependent upon the dose of the imidazoline compound and the intensity/train pulse frequency of reticular stimulation. It was suggested that the two mechanisms may interact with one another in the brainstem and possible modes of interaction were discussed.

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