Modulation of endothelial cell KCa3.1 channels during endothelium-derived hyperpolarizing factor signaling in mesenteric resistance arteries.

Journal article

Arterial hyperpolarization to acetylcholine (ACh) reflects coactivation of K(Ca)3.1 (IK(Ca)) channels and K(Ca)2.3 (SK(Ca)) channels in the endothelium that transfers through myoendothelial gap junctions and diffusible factor(s) to affect smooth muscle relaxation (endothelium-derived hyperpolarizing factor [EDHF] response). However, ACh can differentially activate K(Ca)3.1 and K(Ca)2.3 channels, and we investigated the mechanisms responsible in rat mesenteric arteries. K(Ca)3.1 channel input ...

Expand abstract

Authors: Dora, K; Gallagher, N; McNeish, A; Garland, C

• Publication status: Published
• Journal: Circulation research
• Volume: 102
• Issue: 10
• Pages: 1247-1255
• Publication date: 2008-05-01
• DOI: 10.1161/circresaha.108.172379
• EISSN: 1524-4571
• ISSN: 0009-7330
• Language: English
• Keywords: Calcium; Animals; Acetylcholine; Forskolin; Rats; Carbenoxolone; Muscle, Smooth, Vascular; Intermediate-Conductance Calcium-Activated Potassium Channels; Sodium-Potassium-Exchanging ATPase; Vasodilator Agents; Biological Factors; Gap Junctions; Phenylephrine; Vasoconstrictor Agents; Endothelial Cells; Signal Transduction; Mesenteric Arteries; Vasodilation; Membrane Potentials; Natriuretic Peptide, C-Type; Vascular Resistance