O-2-SENSITIVE K-BODY CHEMORECEPTOR CELLS FROM NORMOXIC AND CHRONICALLY HYPOXIC RATS AND THEIR ROLES IN HYPOXIC CHEMOTRANSDUCTION( CURRENTS IN CAROTID)

Carotid body-mediated ventilatory increases in response to acute hypox ia are attenuated in animals reared in an hypoxic environment. Normall y, O-2-sensitive K+ channels in neurosecretory type I carotid body cel ls are intimately involved in excitation of the intact organ by hypoxi a. We have therefore studied K+ channels and their sensitivity to acut e hypoxia (PO2 12-20 mmHg) in type I cells isolated from neonatal rats born and reared in normoxic and hypoxic environments. When compared w ith cells from normoxic rats, K+ current density in cells from hypoxic rats was significantly reduced, whereas Ca2+ current density was unaf fected. Charybdotoxin (20 nM) inhibited K+ currents in cells from norm oxic rats by approximate to 25% but was without significant effect in cells from hypoxic rats. However, hypoxia caused similar, reversible i nhibitions of K+ currents in cells from the two groups. Resting membra ne potentials (measured at 37 degrees C using the perforated-patch tec hnique) were similar in normoxic and hypoxic rats. However, although a cute hypoxia depolarized type I cells of normoxic rats, it was without effect on membrane potential in type I cells from hypoxic animals. Ch arybdotoxin (20 nM) also depolarized tells from normoxic rats. Our res ults suggest that type I cells from chronically hypoxic rats, like nor moxic rats, possess O-2-sensing mechanisms. However, they lack charybd otoxin-sensitive K+ channels that contribute to resting membrane poten tial in normoxically reared rats, and this appears to prevent them fro m depolarizing (and hence triggering Ca2+ influx and neurosecretion) d uring acute hypoxia.