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Vascul Pharmacol. 2010 Sep-Oct;53(3-4):122-9. doi: 10.1016/j.vph.2010.05.001. Epub 2010 May 12.

Activation of endothelial BKCa channels causes pulmonary vasodilation.

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Vascular Research Laboratory, Providence VA Medical Center, Providence, RI 02908, USA.



Large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels cause hyperpolarization and can regulate vascular tone. In this study, we evaluated the effect of endothelial BK(Ca) activation on pulmonary vascular tone.


The presence of BK(Ca) channels in lung microvascular endothelial cells (LMVEC) and rat lung tissue was confirmed by RT-PCR, immunoblotting and immunohistochemistry. Isolated pulmonary artery (PA) rings and isolated ventilated-perfused rat lungs were used to assay the effects of BK(Ca) channel activation on endothelium-dependent vasodilation.


Immunoblotting and RT-PCR revealed the presence of BK(Ca) channel alpha- and beta(4)-subunits in LMVEC. Immunohistochemical staining showed BK(Ca) channel alpha-subunit expression in vascular endothelium in rat lungs. In arterial ring studies, BK(Ca) channel activation by NS1619 enhanced endothelium-dependent vasodilation that was attenuated by tetraethylammonium and iberiotoxin. In addition, activation of BK(Ca) channels by C-type natriuretic peptide caused endothelial-dependent vasodilation that was blocked by iberiotoxin, L-NAME, and lanthanum. Furthermore, BK(Ca) activation by NS1619 caused a dose-dependent reduction in PA pressures that was attenuated by L-NAME. In vitro, BK(Ca) channel activation in LMVEC caused hyperpolarization and increased NO production.


Pulmonary endothelium expresses BK(Ca) channels. Activation of endothelial BK(Ca) channels causes hyperpolarization and NO mediated endothelium-dependent vasodilation in micro- and macrovasculature in the lung.

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