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

Abstract Whole-cell recordings were used to investigate the effects of a 3-week period of hypoxia (10% O 2 ) on the properties of K + and Ca 2+ 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 Ca 2+ -dependent and Ca 2+ -independent components by bath application of 200 μM Cd 2+ , which blocked Ca 2+ currents and therefore, indirectly, Ca 2+ -dependent K + currents. Ca 2+ -dependent K + current density was not significantly different in control and chronically hypoxic type I cells. Cd 2+ -resistant (Ca 2+ -insensitive) K + current densities were significantly reduced in type I cells from chronically hypoxic rats. Acute hypoxia (Po 2 15–22 mmHg) caused reversible, selective inhibition of Ca 2+ -dependent K + currents in both groups of cells and Ca 2+ -insensitive K + currents were unaffected by acute hypoxia. Ca 2+ channel current density was not significantly affected by chronic hypoxia, nor was the degree of Ca 2+ channel current inhibition caused by nifedipine (5 μM). Acute hypoxia did not affect Ca 2+ channel currents in either group. Our results indicate that adult rat type I cells undergo a selective suppression of Ca 2+ -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.