Effect of carbon dioxide on autonomic cardiovascular responses to systemic hypoxia in conscious rats.
The contribution of the autonomic nervous system to the cardiovascular response to hypoxia with different levels of CO2 was investigated in conscious rats. Wistar rats were chronically instrumented for measurement of arterial blood pressure (ABP), electrocardiogram, and renal sympathetic nerve activity (RSNA). They were exposed to 1) hypocapnic hypoxia (Hypo), 2) isocapnic hypoxia (Iso), and 3) hypercapnic hypoxia (Hyper). Hypo caused a decrease in ABP, an increase in heart rate (HR) and RSNA, and a slight increase in plasma norepinephrine (NE). Iso caused no significant change in ABP or HR but did cause an increase in RSNA and plasma NE. Hyper caused an increase in ABP, a decrease in HR, and an increase in RSNA and plasma NE. In sinoaortic-denervated (SAD) rats, ABP and RSNA decreased and HR tended to decrease during Iso. SAD abolished the bradycardic response during Hyper. Atropine abolished the bradycardic response during Hyper, and HR tended to increase during all three kinds of hypoxia. In all three kinds of hypoxia, ABP and renal sympathetic nervous responses in atropine-treated rats were not significantly different from those in intact rats. These results indicate that Hypo causes sympathetic activation and parasympathetic inhibition while Iso and Hyper cause sympathetic and parasympathetic activation via peripheral chemoreceptors. The MABP-RSNA curve tended to shift to the left and the maximum gain of the baroreflex response tended to decrease during Hypo. In contrast, this curve shifted to the right and the maximum gain of the baroreflex response increased during Iso and Hyper, suggesting that baroreflex function is affected by arterial CO2 levels. We concluded that cardiovascular responses during hypoxia are modified by arterial Pco2 levels and mediated by the autonomic nervous system.
Hirakawa
H
H
Department of Systems Physiology, University of Occupational and Environmental Health, Kitakyushu, Japan.
Nakamura
T
T
Hayashida
Y
Y
D000818:Animals; D001285:Atropine / Q000494:pharmacology; D001341:Autonomic Nervous System / Q000187:drug effects* / Q000503:physiopathology*; D001794:Blood Pressure; D002245:Carbon Dioxide / Q000494:pharmacology*; D002319:Cardiovascular System / Q000187:drug effects; D003714:Denervation; D005740:Gases / Q000097:blood; D006329:Heart Conduction System / Q000187:drug effects* / Q000503:physiopathology*; D000860:Hypoxia / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation; D008297:Male; D009638:Norepinephrine / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D012119:Respiration; D012850:Sinus of Valsalva / Q000294:innervation; D013564:Sympathetic Nervous System / Q000503:physiopathology
D005740:Gases; D002245:Carbon Dioxide; D001285:Atropine; D009638:Norepinephrine