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 μM 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 μM). 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.