Abstract

The adrenergic mechanisms involved in the sinus tachycardia which follows the termination of vagal stimulation ("postvagal tachycardia") were studied in the anesthetized dog. The following results were obtained. Postvagal tachycardia: 1) is not affected by ventricular or atrial drive; 2) is enhanced by the application of either norepinephrine or dopamine on the sinus node area; 3) is increased in magnitude and duration by the catecholamine uptake blockers desipramine and phenoxybenzamine; 4) is significantly reduced by beta blockade with propranolol; 5) is not affected by alpha blockade with phentolamine or dopaminergic blockade with haloperidol; 6) is not affected by Disulfiram, a drug which inhibits dopamine beta-hydroxylase and thereby increases endogenous dopamine; 7) rises more slowly to a smaller peak after bretylium; and 8) is enhanced by phenoxybenzamine, but not by desipramine, after destruction of sympathetic nerves by 6-hydroxydopamine. It is concluded that release of catecholamines by vagally liberated acetylcholine is involved in postvagal tachycardia. The released catecholamine acts on beta but not alpha or dopamine receptors. Catecholamines released from sympathetic nerves may account for an initial component in postvagal tachycardia, but catecholamine(s) released from extraneuronal stores account for most of postvagal tachycardia.