ADRENERGIC-MECHANISMS IN POSTVAGAL TACHYCARDIA

  • 1 January 1979
    • journal article
    • research article
    • Vol. 210  (1) , 56-63
Abstract
The adrenergic mechanisms involved in the sinus tachycardia which follows the termination of vagal stimulation (postvagal tachycardia) were studied in the anesthetized dog. Apparently, postvagal tachycardia: is not affected by ventricular or atrial drive; is enhanced by the application of either norepinephrine or dopamine on the sinus node area; is increased in magnitude and duration by the catecholamine uptake blockers desipramine and phenoxybenzamine; is significantly reduced by .beta.-blockade with propranolol; is not affected by .alpha.-blockade with phentolamine or dopaminergic blockade with haloperidol; is not affected by Disulfiram, a drug which inhibits dopamine .beta.-hydroxylase and thereby increases endogenous dopamine; rises more slowly to a smaller peak after bretylium; and is enhanced by phenoxybenzamine, but not by desipramine, after destruction of sympathetic nerves by 6-hydroxydopamine. Catecholamine release 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.