- Record: found
- Abstract: found
- Article: not found
Genetic deficit of SK3 and IK1 channels disrupts the endothelium-derived hyperpolarizing factor vasodilator pathway and causes hypertension.
Sebastian Brähler
1 ,
Anuradha Kaistha ,
Volker J Schmidt ,
Stephanie E Wölfle ,
Christoph Busch ,
Brajesh P Kaistha ,
Michael Kacik ,
Anna-Lena Hasenau ,
Ivica Grgic ,
Han Si ,
Chris T Bond ,
John P Adelman ,
Heike Wulff ,
Cor de Wit ,
Joachim Hoyer ,
Ralf Köhler
May 05 2009
There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.
Abstract
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.