From a study on the interrelationship between electroshock-induced convulsions, autonomie function, catecholamines, and cardiovascular homeostasis in dogs, the authors found that: (1) the asystole of electroshock (ES) was significantly prolonged by high spinal anesthesia but not by relative alpha- or beta-adrenergic blockade; (2) increased levels of circulating catecholamines were solely responsible for the marked hypertensive response to ES, since the pressor effect could be blocked by preventing the release of catecholamines with high spinal anesthesia or by inhibiting alpha-adrenergic receptors with phenoxybenzamine; (3) the adrenal medulla appeared to be the source of most of the ES-induced increase in circulating catecholamines; (4) the asystole and arrhythmias of ES were a cholinergic effect, since they were blocked by atropine; (5) there was a dose-response relationship between the coulombs of electricity administered and the catecholamine and cardiovascular responses; and (6) that the adverse cardiovascular effects of ES therapy could be ameliorated pharmacologically.