Abstract

The amplitude of reduction in heart rate induced by vagal stimulation is greater when the background level of sympathetic tone is increased (accentuated antagonism). Both pre- and postsynaptic muscarinic mechanisms have been proposed to account for this phenomenon. We attempted to clarify the relative importance of each mechanism by comparing the magnitude of vagal bradycardia during neurally induced tachycardia with that during nonneurally induced tachycardia in the anesthetized dog. Graded tachycardia was induced by raising the stimulus frequency of cardiac sympathetic nerve stimulation stepwise from 1 to 3 and 5 and 10 Hz, and it was also induced by norepinephrine infusion (0.3-10 micrograms/min into the right coronary artery), isoproterenol infusion (0.1 and 0.3 micrograms/kg/min i.v.) and glucagon injection (3-30 micrograms/kg i.v.). The magnitude of the bradycardia produced by vagal nerve stimulation at 3 Hz was determined during the resting state and during the tachycardic state produced by cardiac nerve stimulation and by drug administration. The magnitude of vagal bradycardia was greater during tachycardic state than during the resting state regardless of the means through which tachycardia was produced. Vagal bradycardia during norepinephrine or isoproterenol infusion was of the same magnitude as that during the cardiac sympathetic nerve stimulation when they were compared at the same heart rate. Vagal bradycardia during the glucagon-induced tachycardia was greater than that which occurred during sympathetic tachycardia. Temporary bradycardia resulting from a single-pulse vagal nerve stimulation was augmented markedly during the cardiac sympathetic nerve stimulation, whereas a 2-sec interruption of the cardiac sympathetic nerve stimulation did not alter the sustained tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)