Vagus Nerves and Baroreceptor Control of Ventricular Performance

In innervated, isovolumetric left ventricle preparations, sudden elevations of pressure in the isolated carotid sinus elicited a 9.5% depression of left ventricular systolic pressure (LVSP). After blockade of sympathetic neuroeffector junctions by bretylium tosylate, equivalent intrasinusal pressure changes evoked a 6.8% reduction of LVSP. This response could be completely abolished by atropine sulfate or by cooling the cervical vagi. Therefore, under the conditions of the present experiments, the vagus nerves mediated a significant fraction of the reflex depression of ventricular performance induced by carotid sinus baroreceptor stimulation. An appreciable elevation of LVSP was produced by atropine and by vagal cooling after blockade of sympathetic junctions. This enhancement of ventricular performance is an indication of a tonic negative inotropic influence of the vagus nerves upon the ventricular myocardium.