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School of Physiology and Pharmacology, University of New South Wales, Kensington, Sydney, Australia.

1. It is known that stimulation of the sympathetic cardioaccelerator nerve is followed by prolonged inhibition of cardiac vagal action. This prolonged inhibitory action of the sympathetic nerve is not blocked by alpha- or beta-adrenoceptor blockade, and is not duplicated by administration of noradrenaline. It has been proposed that it is due to the release of neuropeptide Y (NPY) from the sympathetic nerve terminals (Potter, 1984, 1985). 2. The present experiments examined whether prolonged inhibition of cardiac vagal action could be preferentially produced by sympathetic stimulation of different temporal distribution. The experiments were performed on anaesthetized, vagotomized dogs, with pharmacological beta-adrenoceptor blockade. 3. In six animals intermittent supramaximal sympathetic stimulation at 20 Hz (1/2 s stimulation, 1/2 s off; train duration 2 min; total 1200 stimuli) produced significantly greater inhibition (P less than 0.01) of cardiac vagal action than did continuous stimulation at 5 Hz (stimulus duration 4 min; 1200 stimuli). 4. In another series the same total period of stimulation (2.5 min; 1200 stimuli) was used and it was found that intermittent sympathetic stimulation of 16 Hz (1/2 s stimulation, 1/2 s off) produced significantly greater cardiac vagal inhibition (P less than 0.02) than continuous stimulation at 8 Hz. In this case the mean frequency of stimulation was constant but the higher peak stimulation frequency attenuated cardiac vagal action more effectively.