Title: Endothelium-Dependent Hyperpolarization and Potassium Channels
Abstract: In response to various neurohumoral mediators and physical stimuli, the endothelium elicits relaxations or contractions of the underlying vascular smooth muscle. Endothelium-dependent relaxations can be mediated by the release of the endothelium-derived nitric oxide and prostacyclin [1-2]. In addition, endothelial cells release a yet unidentified endothelium-derived hyperpolarizing factor (EDHF), which causes membrane hyperpolarization by opening potassium channels in vascular smooth muscle [3-4]. However, the possibility that EDHF may contribute to endothelium-dependent hyperpolarization and the mechanism underlying this response is the subject of some controversy. Since both NO and some synthesized prostanoids [5] can cause membrane hyperpolarization under certain conditions, depending on the tissues and/or the species studied, the electrophysiological changes attributed to EDHF have to be distinguished from those of either NO or prostanoids by demonstrating its occurrence during combined inhibition of NO synthase and cyclooxygenase [6]. This brief review focuses on endothelium-dependent hyperpolarizations which cannot be attributed to the release of nitric oxide or prostanoids.
Publication Year: 1995
Publication Date: 1995-01-01
Language: en
Type: book-chapter
Indexed In: ['crossref']
Access and Citation
Cited By Count: 2
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