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Inositol 1,4,5-Trisphosphate Receptors in Endothelial Cells Play an Essential Role in Vasodilation and Blood Pressure Regulation.

Background Endothelial NO synthase plays a central role in regulating vasodilation and blood pressure. Intracellular Ca2+ mobilization is a critical modulator of endothelial NO synthase function, and increased cytosolic Ca2+ concentration in endothelial cells is able to induce endothelial NO synthase phosphorylation. Ca2+ release mediated by 3 subtypes of inositol 1,4,5-trisphosphate receptors ( IP 3 Rs) from the endoplasmic reticulum and subsequent Ca2+ entry after endoplasmic reticulum Ca2+ store depletion has been proposed to be the major pathway to mobilize Ca2+ in endothelial cells. However, the physiological role of IP 3 Rs in regulating blood pressure remains largely unclear. Methods and Results To investigate the role of endothelial IP 3 Rs in blood pressure regulation, we first generated an inducible endothelial cell-specific IP 3 R1 knockout mouse model and found that deletion of IP 3 R1 in adult endothelial cells did not affect vasodilation and blood pressure. Considering all 3 subtypes of IP 3 Rs are expressed in mouse endothelial cells, we further generated inducible endothelial cell-specific IP 3 R triple knockout mice and found that deletion of all 3 IP 3 R subtypes decreased plasma NO concentration and increased basal blood pressure. Furthermore, IP 3 R deficiency reduced acetylcholine-induced vasodilation and endothelial NO synthase phosphorylation at Ser1177. Conclusions Our results reveal that IP 3 R-mediated Ca2+ release in vascular endothelial cells plays an important role in regulating vasodilation and physiological blood pressure.

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