The mechanical and hemodynamic components of a cardiogenic hypertensive chemoreflex were studied in 50 dogs. Within 6 seconds after a single injection of serotonin (100 μg/ml) into the left atrium, mean pressure (mm Hg) rose in the aorta from 103 to197 and in the pulmonary artery from 21 to 34. Left ventricular dp/dt virtually doubled. There was an increase (75%) in peripheral vascular resistance that returned to control within 10 seconds. There was no significant change in pulmonary vascular resistance. Aortic and pulmonary arterial hypertension were associated with a profound depression (82%) in atrial force. Atropine transformed this negative inotropic effect on the atria into a positive inotropic action that averaged 65%. In contrast, ventricular force was always sharply increased, more in the right (95%) than in the left ventricle (50%). Bilateral stellectomy did not eliminate the reflex but it completely abolished the initial increase of cardiac contractility; a delayed increase in contractility persisted and was due exclusively to release of catecholamines from the adrenal glands. This cardiogenic hypertensive chemoreflex uses the vagus for its afferent neural traffic and both the sympathetic and the vagus nerves for its efferent route. The brief and intense systemic vasoconstriction concomitant with an increase in cardiac contractility might represent a kind of 'aortic cough'. Some possible clinical implications are discussed.