Science· 2012Q1
Elementary Ca <sup>2+</sup> Signals Through Endothelial TRPV4 Channels Regulate Vascular Function
- 548citations
- Q1SCImago
- 2012year
Short summary
Local Ca2+ signals ('sparklets') through single TRPV4 channels in endothelial cells cause maximal vasodilation by activating IK and SK potassium channels.
AI-generated from the title and abstract; the full text is not read.
Key points
- Identified 'sparklets' as local Ca2+ signals from single TRPV4 channels in vascular endothelium.
- Cooperative gating of TRPV4 channels, with as few as three active, causes maximal vasodilation.
- Vasodilation is mediated by activation of endothelial IK and SK potassium channels.
- TRPV4 sparklets also mediate endothelial-dependent muscarinic receptor signaling.
AI-generated from the title and abstract; the full text is not read.
Abstract
Major 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.
The authors' abstract, as published at the source. Science, 2012 · DOI ↗
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Field: Sensory Systems
Sensory SystemsNeuroscience