1. Rat pups were gestated and born in normoxia (inspired O2 pressure 149 mmHg) or chronic hypoxia (inspired O2 pressure 80 mmHg) to test whether chronic hypoxia alters carotid body glomus cell calcium currents. Carotid bodies were removed from 5- to 8-day-old pups under halothane anesthesia, at which time blood hematocrits averaged 52 ± 1% (mean ± SE) in the chronically hypoxic pups and 36 ± 1% in the normoxic pups (P < 0.05). Glomus cells were then enzymatically isolated from the carotid bodies, and calcium currents were recorded with whole cell patch clamp. 2. Compared with normoxic glomus cells (n = 29), chronically hypoxic glomus cells (n = 32) superfused with 10 mM CaCl2 had larger peak calcium current (146 ± 16 pA vs. 49 ± 7 pA, P < 0.05), larger peak calcium current density t (12.0 ± 1.1 pA/pF vs. 7.3 ± 1.0 pA/pF, P < 0.05), and larger membrane capacitance (12.1 ± 0.9 pF vs. 7.5 ± 0.6 pF, P < 0.05). 3. Threshold for calcium current activation was approximately -40 mV. Currents showed little inactivation during 45-ms test pulses and were half-inactivated by a steady holding voltage of -11 ± 2 mV (n = 15). Currents were reduced 43 ± 13% by 50 μM nifedipine (n = 6, P < 0.05), and were augmented with barium as the charge carrier. These properties suggest that glomus cell calcium current is carried in part through L-type channels, and that it is relatively resistant to steady-state inactivation. 4. Augmented calcium influx through voltage-gated channels in glomus cells from chronically hypoxic neonatal rats may increase carotid body excitability through increased stimulus-secretion coupling. Overall, acclimatization to chronic hypoxia is known to depress acute hypoxic ventilatory reflex responses in neonates. The observations reported here suggest that inhibition of ventilatory reflexes by chronic hypoxia in neonates occurs centrally rather than peripherally.
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