Efferent mechanisms responsible for the bradycardia produced by lesions coinciding with the A1 group of central catecholamine neurons in the conscious rabbit.

The effector mechanisms responsible for the bradycardia evoked by bilateral lesions of the brainstem coinciding with the A1 catecholamine cells were analyzed in four groups of rabbits. Sham or lesion operations were carried out in animals with intact cardiac effectors, with cardiac sympathetic block induced by propranolol, with cardiac vagal block induced by methylscopolamine and with total cardiac autonomic block induced by the use of both drugs together. Lesions produced a transient increase in blood pressure of 25 (s.e.m. = 4) mmHg and a transient bradycardia, or increase in heart period of 141 (s.e.m. = 18) ms. The bradycardia had both baroreflex-independent and baroreflex-dependent components as determined from analysis of stimulus response curves relating heart period to mean arterial pressure. The 'baroindependent' component of the bradycardia, measured as a lengthening in heart period, ranged from 35-49 ms in the four groups of animals and was unaffected by administration of propranolol alone, methylscopolamine alone, or of both together. These findings suggest that the baroindependent slowing of the heart is not mediated through changes in activity of either the cardiac sympathetic nerves or of the vagal fibres innervating the heart. The 'baroreceptor' component of the bradycardia reflects that portion of the decrease in heart rate resulting directly from the increase in blood pressure. This component was found to account for a lengthening in the heart period of 81 (s.e.m. = 23) ms in animals with intact effector mechanisms: it was virtually abolished by methylscopolamine (0 ms, s.e.m. = 13) but not significantly affected by propranolol (54 ms, s.e.m. = 25), indicating that this barodependent component is predominantly mediated through the vagus.