Review
Endothelium-dependent hyperpolarization: a role in the control of vascular tone

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Abstract

Endothelial-dependent relaxation of vascular smooth muscle cells evoked by a number of agonists, including cholinomimetics and substance P, is often accompanied by an increase (repolarization and/or hyperpolarization) in the membrane potential. This change in membrane potential appears predominately to reflect the action of an endothelial-derived hyperpolarizing factor (EDHF), which is distinct from NO (or endothelial-derived relaxing factor), and is discussed in this article by Chris Garland and colleagues. In large conducting arteries, EDHF may provide a secondary system to NO, which assumes primary importance in some disease states such as pulmonary hypertension and atherosclerosis. However, in small resistance arteries (100–300 μm), EDHF appears to be a major determinant of vascular calibre under normal conditions, and may therefore be of primary importance in the regulation of vascular resistance.

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      Citation Excerpt :

      Endothelial-dependent relaxation of vascular smooth muscle cells evoked by a number of agonists, including cholinomimetics, is often accompanied by an increase in the membrane potential (repolarization and/or hyperpolarization), caused by an endothelial-derived hyperpolarizing factor (EDHF), which is distinct from NO and PGI2. In large conducting arteries, EDHF may provide a secondary system to NO and PGI2, but in small resistance arteries (100–300 microns), it appears to be a major determinant of vascular calibre under normal conditions, and may therefore be of primary importance in the regulation of vascular resistance [125]. In the combined presence of NOS and COX inhibitors, pulse pressure-induced release of EDHF is endothelial-dependent and proportional to the amplitude of the pressure.

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