Abstract
St 155 causes hypotension and bradycardia, actions which have been reported to result from central suppression of sympathetic outflow. Our objective was to determine if increased vagal activity might contribute to the bradycardia. Using anesthetized dogs with cardiac sympathetic function abolished by adrenergic neurone or beta-blockade, it was found that St 155 caused a bradycardia which was overcome by atropine or bilateral vagotomy. In such dogs the tachycardias or null effects of adrenaline and noradrenaline became bradycardias after St 155, and reverted to pre-St 155 responses after bilateral vagotomy, carotid sinus denervation or atropine. St 155 did not alter responses to peripheral vagal stimulation or have any beta-adrenergic blocking activity. Our data suggests that St 155 may enhance vagal activity such that resting heart rate is lowered and compensatory reflexes initiated by adrenaline and noradrenaline pressor responses may predominate over the positive chronotropic activity of these amine.
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