20-Hydroxyeicosatetraenoic acid potentiates contractile activation of canine basilar artery in response to stretch via protein kinase Calpha-mediated inhibition of calcium-activated potassium channel.

Abstract

Blood vessels are persistently exposed to hemodynamic forces in the form of pressure and flow. The vascular smooth muscle contracts in response to stretch/increased intraluminal pressure, and dilates in response to release/decreased intraluminal pressure (Bayliss, 1902). This autoregulatory response is myogenic in nature, and is called “Bayliss effect.” To the contrary, flow/shear stress-dependent dilatation, so called “Schrezenmayar effect” (1933), caused by released vasodilators including nitric oxide from vascular endothelium or other components, can physiologically counteract the myogenic contraction. The cerebral artery is particularly sensitive to pressure and stretch, and shows myogenic contraction (Nakayama et al., 2002). Furthermore, we previously reported that large conductance Ca2+-activated K+ channel (KCa channel) blockers, including iberiotoxin, charybdotoxin, and tetraethylammonium, sensitized the canine basilar artery to mechanical stretch (Obara et al., 2001).KeywordsCytochrome P450 MonooxygenaseEpoxyeicosatrienoic AcidVascular Smooth Muscle ContractCoronary Artery Smooth Muscle CellCanine Basilar ArteryThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.