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• W2024103448 abstract "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 Ca 2 + concentration ([Ca 2 + ] 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 [Ca 2 + ] 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." @default.
• W2024103448 created "2016-06-24" @default.
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• W2024103448 date "2003-10-01" @default.
• W2024103448 modified "2023-09-23" @default.
• W2024103448 title "Role of endothelial intermediate conductance K_Cachannels in cerebral EDHF-mediated dilations" @default.
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• W2024103448 doi "https://doi.org/10.1152/ajpheart.00376.2003" @default.
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