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Department of Physiology, New York Medical College, Valhalla, New York 10595; and Department of Pathophysiology, Semmelweis University, 1445 Budapest, Hungary
In skeletal muscle arterioles, the pathway leading to non-nitric oxide (NO), non-prostaglandin-mediated endothelium-derived hyperpolarizing factor (EDHF)-type dilations is not well characterized. To elucidate some of the steps in this process, simultaneous changes in endothelial intracellular Ca2+ concentration ([Ca2+]i) and the diameter of rat gracilis muscle arterioles (~60 µm) to acetylcholine (ACh) were measured by fura 2 microfluorimetry (in the absence of NO and prostaglandins). ACh elicited rapid increases in endothelial [Ca2+]i (101 ± 7%), followed by substantial dilations (73 ± 2%, coupling time: 1.3 ± 0.2 s) that were prevented by endothelial loading of an intracellular Ca2+ chelator [1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid]. Arteriolar dilations to ACh were also inhibited by intraluminal administration of the Ca2+-activated K+ (KCa) channel blockers charybdotoxin plus apamin or by palmitoleic acid, an uncoupler of myoendothelial gap junctions without affecting changes in endothelial [Ca2+]i. The presence of large conductance KCa channels on arteriolar endothelial cells was demonstrated with immunohistochemisty. We propose that in skeletal muscle arterioles, EDHF-type mediation is evoked by an increase in endothelial [Ca2+]i, which by activating endothelial KCa channels elicits hyperpolarization that is conducted via myoendothelial gap junctions to the smooth muscle resulting in decreases in [Ca2+]i and consequently dilation.
endothelium-dependent hyperpolarizing factor; arteriolar endothelium; potassium channels; charybdotoxin
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