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% O-2) on the properties of K+ and Ca2+ currents in type I cells isolated from adult rat carotid bodies. Chronic hypox ia significantly increased whole-cell membrane capacitance. K+ current amplitudes were not affected by this period of hypoxia, but K+ curren t 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+-independe nt components by bath application of 200 mu M Cd2+, which blocked Ca2 currents and therefore, indirectly, Ca2+-dependent K+ currents. Ca2+- dependent K+ current density was not significantly different in contro l and chronically hypoxic type I cells. Cd2+ resistant (Ca2+-insensiti ve) K+ current densities were significantly reduced in type I cells fr om chronically hypoxic rats. Acute hypoxia(Po-2 15-22 mmHg) caused rev ersible, selective inhibition of Ca2+-dependent K+ currents in both gr oups of cells and Ca2+-insensitive K+ currents were unaffected by acut e hypoxia. Ca2+ channel current density was not significantly affected by chronic hypoxia, nor was the degree of Ca2+ channel current inhibi tion caused by nifedipine (5 mu M). Acute hypoxia did not affect Ca2channel currents in either group. Our results indicate that adult rat type I cells undergo a selective suppression of Ca2+ insensitive, volt age-gated K+ currents in response to chronic hypoxia in vivo. These fi ndings are discussed in relation to the known adaptations of the intac t carotid body to chronic hypoxia. (C) 1998 Elsevier Science B.V. All rights reserved.