Baroreflex-mediated cardiovascular responsesto hyperbaric oxygen. J Appl Physiol 115: 819–828, 2013.First published July 3, 2013; doi:10.1152/japplphysiol.00625.2013.—The cardiovascular system responds to hyperbaric hyperoxia (HBO2)with vasoconstriction, hypertension, bradycardia, and reduced cardiacoutput (CO). We tested the hypothesis that these responses are linkedby a common mechanism—activation of the arterial baroreflex. Baroreflexfunction in HBO2 was assessed in anesthetized and consciousrats after deafferentation of aortic or carotid baroreceptors or both.Cardiovascular and autonomic responses to HBO2 in these animalswere compared with those in intact animals at 2.5 ATA for consciousrats and at 3 ATA for anesthetized rats. During O2 compression,hypertension was greater after aortic or carotid baroreceptor deafferentationand was significantly more severe if these procedures werecombined. Similarly, the hyperoxic bradycardia observed in intactanimals was diminished after aortic or carotid baroreceptor deafferentationand replaced by a slight tachycardia after complete baroreceptordeafferentation. We found that hypertension, bradycardia, andreduced CO—the initial cardiovascular responses to moderate levelsof HBO2—are coordinated through a baroreflex-mediated mechanisminitiated by HBO2-induced vasoconstriction. Furthermore, we haveshown that baroreceptor activation in HBO2 inhibits sympatheticoutflow and can partially reverse an O2-dependent increase in arterialpressure.