Mechanism of vasopressin-induced bradycardia in dogs.

In dogs anesthetized with intravenous chloralose, vasopressin was injected either intravenously or into the cerebral ventricles, and the cardiovascular effects were studied before and after stabilizing the arterial blood pressure, bilateral vagotomy, and transection of the cervical cord at the level of C2. Intravenous vasopressin caused a rise in arterial blood pressure and pronounced bradycardia. The bradycardia appeared to be partly due to a peripheral depressant action on the heart, probably resulting from coronary constriction and partly from reflex vagal stimulation resulting from the rise in arterial blood pressure. A direct stimulating action of vasopressin on the central cardioinhibitory neurons played only a minor role in the production of the bradycardia. Injections of vasopressin, into either a lateral or the fourth ventricle, produced an insignificant rise in arterial blood pressure but marked bradycardia. A peripheral effect of the vasopressin after its absorption into the blood stream could be excluded as the cause of the bradycardia, since an injection of vasopressin into the cerebral ventricles produced diuresis, not antidiuresis. The bradycardia was more pronounced and occurred earlier when the vasopressin was injected into the fourth rather than into a lateral ventricle. The bradycardia produced by the injection of vasopressin into the cerebral ventricles could be almost fully accounted for by a central stimulating action on the cardioinhibitory neurons in the region of the vagal nuclei, which are closer to the fourth ventricle than to the lateral ventricles. ADDITIONAL