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

Publikation

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

Wissenschaftlicher Artikel/Review - 20.04.2009

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

Zitation

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.

Art

Wissenschaftlicher Artikel/Review (Englisch)

Zeitschrift

Circulation 2009; 119

Veröffentlichungsdatum

20.04.2009

eISSN (Online)

1524-4539

Seiten

2323-32

Kurzbeschreibung/Zielsetzung

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.