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Background— Hypertension, a major cause of cardiovascular morbidity and mortality, can result from chronic hypoxia; however, the pathogenesis of this disorder is unknown. We hypothesized that downregulation of the maxi-K+ channel β1 -subunit by hypoxia decreases the ability of these channels to hyperpolarize arterial smooth muscle cells, thus favoring vasoconstriction and hypertension.Methods and Results— Lowering O2 tension produced a decrease of maxi-K+ β1 -subunit mRNA levels in rat (aortic and basilar) and human (mammary) arterial myocytes. This was paralleled by a reduction of the β1 -subunit protein level as determined by immunocytochemistry and flow cytometry. Exposure to hypoxia also produced a decrease of open probability, mean open time, and sensitivity to the xenoestrogen tamoxifen of single maxi-K+ channels recorded from patch-clamped dispersed myocytes. The number of channels per patch and the single-channel conductance were not altered. The vasorelaxing force of maxi-K+ channels was diminished in rat and human arterial rings exposed to low oxygen tension.Conclusions— These results indicate that a decrease of the maxi-K+ channel β1 -subunit expression in arterial myocytes is a key factor in the vasomotor alterations induced by hypoxia.

Decreased Expression of Maxi-K + Channel β 1 -Subunit and Altered Vasoregulation in Hypoxia

Decreased Expression of Maxi-K ⁺ Channel β ₁ -Subunit and Altered Vasoregulation in Hypoxia