Genetic deficit of SK3 and IK1 channels disrupts the endothelium-derived hyperpolarizing factor vasodilator pathway and causes hypertension.

Publication

Genetic deficit of SK3 and IK1 channels disrupts the endothelium-derived hyperpolarizing factor vasodilator pathway and causes hypertension.

Journal Paper/Review - Apr 20, 2009

Brähler Sebastian, Kaistha Anuradha, Schmidt Volker, Wölfle Stephanie E, Busch Christoph, Kaistha Brajesh P, Kacik Michael, Hasenau Anna-Lena, Grgic Ivica, Siiskonen Hanna, Bond Chris T, Adelman John P, Wulff Heike, de Wit Cor, Hoyer Joachim, Köhler Ralf

Citation

Brähler S, Kaistha A, Schmidt V, Wölfle S, Busch C, Kaistha B, Kacik M, Hasenau A, Grgic I, Siiskonen H, Bond C, Adelman J, Wulff H, de Wit C, Hoyer J, Köhler R. Genetic deficit of SK3 and IK1 channels disrupts the endothelium-derived hyperpolarizing factor vasodilator pathway and causes hypertension. Circulation 2009; 119:2323-32.

Type

Journal Paper/Review (English)

Journal

Circulation 2009; 119

Publication Date

Apr 20, 2009

Issn Electronic

1524-4539

Pages

2323-32

Brief description/objective

It has been proposed that activation of endothelial SK3 (K(Ca)2.3) and IK1 (K(Ca)3.1) K+ channels plays a role in the arteriolar dilation attributed to an endothelium-derived hyperpolarizing factor (EDHF). However, our understanding of the precise function of SK3 and IK1 in the EDHF dilator response and in blood pressure control remains incomplete. To clarify the roles of SK3 and IK1 channels in the EDHF dilator response and their contribution to blood pressure control in vivo, we generated mice deficient for both channels.