Carotid body chemoreception in the absence and presence of CO2-HCO3-.
Carotid body (CB) chemosensory responses to natural and pharmacological stimuli were studied in vitro in the presence and nominal absence of CO2-HCO3- in the perfusion-superfusion media. The CBs obtained from cats (n = 10), anesthetized with sodium pentobarbitone, were simultaneously perfused and superfused with a modified Tyrode solution at 36.5 +/- 0.5 degrees C, equilibrated respectively with PO2 of 120 and less than 20 Torr. The Tyrode, nominally free of CO2-HCO3- (HEPES-NaOH, pH 7.38, 310 mOsm), was used first. Subsequently the Tyrode containing HEPES-HCO3-, equilibrated with PCO2 of 36.8 Torr (pH 7.38) was used. Chemosensory discharges were recorded from the carotid sinus nerve. Both hypoxia (PO2 = 20-25 Torr) and ischemic hypoxia stimulated the discharge in the absence and presence of CO2-HCO3-. However, the presence of CO2-HCO3- significantly raised the baseline activity, augmented the speed, sensitivity and the maximal responses to both types of hypoxia. Hypercapnic perfusate (PCO2 = 65 Torr at pH 7.17) produced a peak response equally promptly in the absence and presence of CO2-HCO3- in the ongoing perfusate but generated a larger and more sustained response. Presence of CO2-HCO3- strongly potentiated the responses to cyanide (10(-10)-10(-7) mol) but less strikingly the responses to nicotine (10(-11)-10(-8) mol). Thus, the extracellular CO2-HCO3- significantly improved the response to hypoxia but was not essential for O2 chemoreception. The underlying mechanisms of the effect of CO2-HCO3- is likely to be mediated by the Cl(-)-HCO3- anion exchanger in the pH regulation of glomus cells.
Iturriaga
R
R
Department of Physiology, School of Medicine, University of Pennsylvania, Philadelphia 19104-6085.
Lahiri
S
S
D000818:Animals; D001639:Bicarbonates / Q000494:pharmacology*; D002245:Carbon Dioxide / Q000494:pharmacology*; D002344:Carotid Body / Q000187:drug effects / Q000502:physiology*; D002415:Cats; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D005260:Female; D000860:Hypoxia; D008297:Male; D009538:Nicotine / Q000494:pharmacology; D010313:Partial Pressure; D010477:Perfusion; D012966:Sodium Cyanide / Q000494:pharmacology; D013997:Time Factors
D001639:Bicarbonates; D002245:Carbon Dioxide; D009538:Nicotine; D012966:Sodium Cyanide