SYMPATHETIC INVOLVEMENT IN VAGAL ESCAPE AND EFFECTS OF BETA-RECEPTOR BLOCKING DRUGS

Vagal escape was initiated in chloralose anaesthetised cats. A sympathetic component is involved in vagal escape. Concomitant β-receptor stimulation produced by sympathomimetic amines or cocaine increased, and blockade of sympathetic effects with β-receptor antagonists or with St-155 (2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride) decreased the rate of vagal escape. Low doses of the β-receptor antagonists propranolol, pronethalol and MJ-1999 which produced specific β-receptor blockade resulted in a decrease in the number of ectopic vagal escape beats. With higher doses there was a further decrease in the number of ectopic escape beats which was associated with the appearance of beats initiated from the sino-atrial node. The latter effects are due to a combination of cardio-depressant and atropinic activities of the drugs. Muscarinic receptor blockade with cumulative doses of atropine produced a reduction in the number of ectopic beats, and a rise in the number of sinus beats during vagal stimulation. Similar results with procainamide are due to a combination of cardio-depressant and ganglion blocking actions. © 1969.