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Direct effect of chronic hypoxia in suppressing large conductance Ca2+‐activated K+ channel activity in ovine uterine arteries via increasing oxidative stress

Chronic hypoxia has a direct effect in down‐regulating the BKCa channel β1 subunit and inhibiting the BKCa channel activity in uterine arteries of pregnant sheep. Oxidative stress plays a causal role in hypoxia‐mediated suppression of BKCa channel function. The steroid hormone‐induced effect on BKCa channels is a target of hypoxia‐mediated oxidative stress. Inhibition of oxidative stress ameliorates the adverse effect of hypoxia both ex vivo and in vivo in pregnant sheep exposed to long‐term high‐altitude hypoxia. Our findings provide novel evidence of a causative role of oxidative stress in hypoxia‐mediated inhibition of the BKCa channel activity in uterine arteries and new insights in understanding and alleviating pregnancy complications associated with gestational hypoxia such as pre‐eclampsia and fetal growth restriction.