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lüll Elementary Ca2+ signals through endothelial TRPV4 channels regulate vascular function Sonkusare SK; Bonev AD; Ledoux J; Liedtke W; Kotlikoff MI; Heppner TJ; Hill-Eubanks DC; Nelson MTScience 2012[May]; 336 (6081): 597-601Major features of the transcellular signaling mechanism responsible for endothelium-dependent regulation of vascular smooth muscle tone are unresolved. We identified local calcium (Ca(2+)) signals ("sparklets") in the vascular endothelium of resistance arteries that represent Ca(2+) influx through single TRPV4 cation channels. Gating of individual TRPV4 channels within a four-channel cluster was cooperative, with activation of as few as three channels per cell causing maximal dilation through activation of endothelial cell intermediate (IK)- and small (SK)-conductance, Ca(2+)-sensitive potassium (K(+)) channels. Endothelial-dependent muscarinic receptor signaling also acted largely through TRPV4 sparklet-mediated stimulation of IK and SK channels to promote vasodilation. These results support the concept that Ca(2+) influx through single TRPV4 channels is leveraged by the amplifier effect of cooperative channel gating and the high Ca(2+) sensitivity of IK and SK channels to cause vasodilation.|*Calcium Signaling[MESH]|*Vasodilation[MESH]|Animals[MESH]|Calcium/*metabolism[MESH]|Endothelial Cells/drug effects/*metabolism/physiology[MESH]|Endothelium, Vascular/drug effects/metabolism/physiology[MESH]|Intermediate-Conductance Calcium-Activated Potassium Channels/metabolism[MESH]|Ion Channel Gating[MESH]|Leucine/analogs & derivatives/pharmacology[MESH]|Mesenteric Arteries/drug effects/*metabolism/physiology[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mice, Transgenic[MESH]|Patch-Clamp Techniques[MESH]|Receptors, Muscarinic/metabolism[MESH]|Signal Transduction[MESH]|Small-Conductance Calcium-Activated Potassium Channels/metabolism[MESH]|Sulfonamides/pharmacology[MESH]|TRPV Cation Channels/agonists/antagonists & inhibitors/*metabolism[MESH] |