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Smooth Muscle to Endothelial Communication in Mesenteric Arteries
Abstract   Peer reviewed

Smooth Muscle to Endothelial Communication in Mesenteric Arteries

P M Kerr, R Tam, C H Tran, Shaun L Sandow, D Welsh and F Plane
FASEB Journal, Vol.25(819.17)
2011
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http://www.fasebj.org/View
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Abstract

Biochemistry and Cell Biology Physiology Medical Physiology smooth muscle endothelial communication mesenteric arteries
Arterial vasoconstriction is limited by the endothelium but how contraction of smooth muscle cells in the vessel wall leads to activation of the endothelium has not been addressed. We propose that inositol 1,4,5 trisphosphate (IP3) generated by vasoconstrictor action crosses myoendoendothelial gap junctions (MEGJs), elicits Ca2+ release from IP3-receptors (IP3R) and activates intermediate conductance Ca2+-activated K+ (IKCa) channels to elicit a negative feedback response. Constriction and depolarization of rat mesenteric arteries to phenylephrine (PE) was enhanced by endothelial removal. Selective application of xestaspongin, an IP3R inhibitor, to the lumen of pressurized arteries, or superfusion with an inhibitor of IKCa channels, enhanced vasoconstriction to PE. Application of PE depolarized the smooth muscle membrane potential but caused a small, significant hyperpolarization of endothelial cell membrane potential. In the presence of IKCa channel block, this hyperpolarization was lost and significant endothelial depolarization to PE was observed. Ca2+ imaging showed that stimulation of smooth muscle cells by PE is associated with discrete, localized increases in Ca2+ within endothelial cells. Ultrastructural studies revealed IP3 receptors and IKCa channels localized at MEGJs in mesenteric arteries. These data indicate that IP3R and IKCa channels are central to endothelium-dependent modulation of vasoconstriction.

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