Ionic currents in carotid body type I cells isolated from normoxic and chronically hypoxic adult rats.

Whole-cell recordings were used to investigate the effects of a 3-week period of hypoxia (10% O2) on the properties of K+ and Ca2+ currents in type I cells isolated from adult rat carotid bodies. Chronic hypoxia significantly increased whole-cell membrane capacitance. K+ current amplitudes were not affected by this period of hypoxia, but K+ current density was significantly reduced in cells from chronically hypoxic rats as compared with normoxically maintained, age-matched controls. K+ current density was separated into Ca2+-dependent and Ca2+-independent components by bath application of 200 microM Cd2+, which blocked Ca2+ currents and therefore, indirectly, Ca2+-dependent K+ currents. Ca2+-dependent K+ current density was not significantly different in control and chronically hypoxic type I cells. Cd2+-resistant (Ca2+-insensitive) K+ current densities were significantly reduced in type I cells from chronically hypoxic rats. Acute hypoxia (Po2 15-22 mmHg) caused reversible, selective inhibition of Ca2+-dependent K+ currents in both groups of cells and Ca2+-insensitive K+ currents were unaffected by acute hypoxia. Ca2+ channel current density was not significantly affected by chronic hypoxia, nor was the degree of Ca2+ channel current inhibition caused by nifedipine (5 microM). Acute hypoxia did not affect Ca2+ channel currents in either group. Our results indicate that adult rat type I cells undergo a selective suppression of Ca2+-insensitive, voltage-gated K+ currents in response to chronic hypoxia in vivo. These findings are discussed in relation to the known adaptations of the intact carotid body to chronic hypoxia.