Experiments were performed on unanesthetized rats (n=6) to determine the systemic hemodynamics during chemoreflex activation by intravenous KCN. Rats chronically instrumented with ultrasonic flow probes in the ascendant aorta were submitted to KCN injections (30 microg/kg) before and after sequential administration of the autonomic blockers atropine and propranolol. In the control period KCN injections produced a 60% reduction in heart rate (HR) and a 46% elevation in blood pressure (BP), while cardiac output (CO) decreased 76%, stroke volume (SV) decreased 40%, and calculated total peripheral resistance (TPR) increased 900%. Atropine administration increased resting HR, whereas no change was observed in CO or BP. Chemoreflex-induced bradycardia was markedly attenuated (26%), and the pressor response was potentiated (59%) after atropine administration. CO and TPR responses were both attenuated after atropine administration (68% and 718%, respectively). Sequential administration of propranolol decreased HR but did not change the cardiovascular responses to KCN injections compared with the responses observed after atropine administration. In conclusion, CO is greatly reduced during KCN-evoked chemoreflex. Besides the intense bradycardia, a decrease in SV contributed to this reduction. Bradycardic response was most dependent on the cardiac parasympathetic activation, and the reduction in SV was probably most dependent on the increased cardiac afterload due to the sudden increase in BP.