Reduction of delayed rectifier K+ current in rat pulmonary artery cells during chronic hypoxia
Chronic hypoxia leads to both structural and functional alterations of the pulmonary vasculature. Although the responsiveness of pulmonary arteries (PA) to endothelium-dependent vasorelaxants (1), the effectiveness of vasorelaxants which act directly or indirectly to reduce Ca2+ influx via voltage-gated channels is increased (9,13). Basal tone also increases. These effects may be due to a persistent depolarization of the resting membrane potential which develops during chronic hypoxia in PAs of > 300 um inner diameter (8,12). Since the membrane potential of vascular smooth muscle is likely to be set mainly by the activity of plasmalemmel K+ channels, we investigated whether K+ currents in smooth muscle cells of small PA differed in rats maintained for 4 weeks under either normoxic of hypoxic conditions. We found that the delayed rectifier K+ current was smaller in PA cells from chronic hypoxic rats compared to normoxic rats.
KeywordsRest Membrane Potential Chronic Hypoxia Pipette Solution Guanosine Diphosphate Rabbit Portal Vein
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