MECHANISMS FOR CARDIAC SLOWING BY METHOXAMINE

The baroreceptors in the carotid sinuses and aortic arch are responsible for the major component of the bradycardiac responses to intravenous injection of methoxamine because selective denervation of both groups of receptors significantly reduces the intensity of the response. Although the stretch receptors of the carotid sinuses can be stimulated by intracarotid injection of methoxamine, the size of the effective intracarotid dose does not warrant the conclusion that this mechanism is important following intravenous injection of the drug. The rise in arterial blood pressure brought about by the constrictor action of the drug on systemic vessels activates the baroreceptors in the sinuses and aortic arch. The slight bradycardiac response which persists after carotid-aortic denervation is not due to direct action of the drug of the medullary centers, sino-auricular node, and on the coronary and pulmonary receptors responsible for the Bezold-Jarisch reflex. The remaining alternative explanation is that stretch receptors in the cardiac wall are activated by rise in auricular and ventricular pressures accompanying the pressor action of methoxamine. No direct evidence for this possibility is offered.