RECIPROCAL PHOTOLABILE O-2 CONSUMPTION AND CHEMORECEPTOR EXCITATION BY CARBON-MONOXIDE IN THE CAT CAROTID-BODY - EVIDENCE FOR CYTOCHROME A(3) AS THE PRIMARY O-2 SENSOR

High carbon monoxide (CO) gas tensions (> 500 Torr) at normoxic PO2 (125-140 Torr) stimulates carotid chemosensory discharge in the perfused carotid body (CB) in the absence but not in the presence of light. According to a metabolic hypothesis of O-2 chemoreception, the increased chemosensory discharge should correspond to a photoreversible decrease of O-2 consumption, unlike a non-respiratory hypothesis. We tested the respiratory vs. non-respiratory hypotheses of O-2 chemoreception in the cat CB by measuring the effect of high CO2 Experiments were conducted using CBs perfused and superfused in vitro with high CO in normoxic, normocapnic cell-free CO2-HCO3- buffer solution at 37 degrees C. Simultaneous measurements of the rate of O-2 disappearance with recessed PO2 microelectrodes and chemosensory discharge were made after flow interruption with and without CO in the perfusate. The control O-2 disappearance rate without CO was -3.66 +/- 0.43 (S.E.) Torr/s (100 measurements in 12 cat CBs). In the dark, high CO reduced the O-2 disappearance rate to -2.35 +/- 0.33 Torr/s, or 64.2 +/- 9.0% of control (P < 0.005, 34 measurements). High CO was excitatory in the dark, with an increase in baseline neural discharge from 129.2 +/- 47.0 to 399.3 +/- 49.1 impulses per s (P < 0.0001), and maximum discharge rate of 659 +/- 76 impulses/s (N.S. compared to control) during now interruption. During perfusion with high CO in the light, there were no significant differences in baseline neural discharge or in the maximum neural discharge after now interruption, and little effect on O-2 metabolism (88.8 +/- 11.5% of control, N.S., 29 measurements). Thus the photoreversible decrease of O-2 consumption and chemosensory excitation in the CO-treated CB is consistent with the metabolic theory of O-2 chemoreception.