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Role of endothelial intermediate conductance K_Ca channels in cerebral EDHF-mediated dilations

Department of Anesthesiology, Baylor College of Medicine, Houston, Texas 77030

Submitted 22 April 2003 ; accepted in final form 11 June 2003

The present study evaluated the role of endothelial intermediate conductance calcium-sensitive potassium channels (IK_Ca) in the mechanism of endothelium-derived hyperpolarizing factor (EDHF)-mediated dilations in pressurized cerebral arteries. Male rat middle cerebral arteries (MCA) were mounted in an isolated vessel chamber, pressurized (85 mmHg), and luminally perfused (100 µl/min). Artery diameter was measured simultaneously with either endothelial intracellular Ca²⁺ concentration ([Ca²⁺]_i; fura-2) or changes in endothelial membrane potential [4-{2-[6-(dioctylamino)-2-naphthalenyl]ethenyl}1-(3-sulfopropyl)-pyridinium (di-8-ANEPPS)]. Nitric oxide synthase and cyclooxygenase inhibitors were present throughout. Luminal application of UTP produced EDHF-mediated dilations that correlated with significant endothelial hyperpolarization. The dilation and endothelial hyperpolarization were virtually abolished by inhibitors of IK_Ca channels but not by selective inhibitors of small or large conductance K_Ca channels (apamin and iberiotoxin, respectively). Additionally, direct stimulation of endothelial IK_Ca channels with 1-ethyl-2-benzimidazolinone (1-EBIO) produced endothelial hyperpolarization and vasodilatation that were blocked by inhibitors of IK_Ca channels. 1-EBIO hyperpolarized the endothelium but did not affect endothelial [Ca²⁺]_i. We conclude that the mechanism of EDHF-mediated dilations in cerebral arteries requires stimulation of endothelial IK_Ca channels to promote endothelial hyperpolarization and subsequent vasodilatation.

calcium; brain; purinergic; small conductance potassium channels; large conductance potassium channels; endothelium-derived hyperpolarizing factor

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