Abstract
1. In order to understand better the relationship between sinus nerve chemoreceptor activity and changes in glomus cell membrane current, both were measured simultaneously in rat carotid bodies in vitro. Mean membrane resistance of intact glomus cells was 1327 +/- 140 M omega (n = 104, mean +/- S.E.M.) and membrane capacitance was 7.9 +/- 0.8 pF (n = 28). 2. Over the course of 15 min following the start of whole-cell recording, outward current increased by 169 +/- 48% (n = 19), but there was no significant change in holding current or membrane resistance. Reversal potential of the tail current was not changed over this time period. Current run-up was not affected by addition of ATP, Ca2+, okadaic acid or H-7 to the pipette fluid. 3. Brief hypoxia (30-45 s duration, 0 mmHg at nadir) caused a rapid increase in nerve activity, but, on average, no significant change in cell holding current, or resistance. Outward current slightly decreased during hypoxia but failed to recover in the post-hypoxia period. 4. Tetraethylammonium (20 mM), and 4-aminopyridine (1 mM) reduced the outward current to 54 +/- 7 and 66 +/- 3% of control, respectively, but basal nerve activity was unchanged and the nerve response to hypoxia remained intact. 5. These results suggest that hypoxia modulation of glomus cell K+ current is not the primary initiating factor in the nerve response to brief periods of hypoxia in the rat carotid body.