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Open AccessJournal ArticleDOI

TRPC3 is involved in flow- and bradykinin-induced vasodilation in rat small mesenteric arteries.

TLDR
The results suggest that TRPC3 is involved in flow- and bradykinin-induced vasodilation in rat small mesenteric arteries probably by mediating the Ca2+ influx into endothelial cells.
Abstract
To test the possible involvement of TRPC3 in agonist-induced relaxation and flow-induced vasodilation in rat small mesenteric arteries. Male Sprague-Dawley rats were used in the present study. After 72 h-treatment of antisense oligo via tail vein injection, isometric tension and isobaric diameter measurement were carried out with isolated mesenteric artery segments by using either a Pressure Myograph or a Multi Myograph system. Endothelial [Ca2+]i changes were measured with a MetaFluor imaging system in response to flow or to 30 nmol/L bradykinin. Immunohistochemical study showed that the 72 h-treatment of antisense oligo via tail vein injection markedly decreased the TRPC3 expression in mesenteric arteries, indicating the effectiveness of the antisense oligo. Isometric tension and isobaric diameter measurement showed that, although the antisense oligo treatment did not affect histamine-, ATP-, and CPA-induced relaxation, it did reduce the magnitude of flow-induced vasodilation by approximately 13% and decreased bradykinin-induced vascular relaxation with its EC50 value raised by nearly 3-fold. Endothelial [Ca2+]i measurement revealed that treatment of the arteries with antisense oligos significantly attenuated the magnitude of endothelial [Ca2+]i rise in response to flow and to 30 nmol/L bradykinin. The results suggest that TRPC3 is involved in flow- and bradykinin-induced vasodilation in rat small mesenteric arteries probably by mediating the Ca2+ influx into endothelial cells.

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Journal ArticleDOI

Transient Receptor Potential Channels in the Vasculature

TL;DR: The mammalian genome encodes 28 distinct members of the transient receptor potential (TRP) superfamily of cation channels, which exhibit varying degrees of selectivity for different ionic species, including sensory perception and signal transduction.
Journal ArticleDOI

Physiology and pathophysiology of canonical transient receptor potential channels

TL;DR: This analysis reveals TRPCs as major and unsuspected gates of Ca2+ entry that contribute, depending on context, to activation of transcription factors, apoptosis, vascular contractility, platelet activation, and cardiac hypertrophy, as well as to normal and abnormal cell proliferation.
Journal ArticleDOI

Update on vascular endothelial Ca(2+) signalling: A tale of ion channels, pumps and transporters.

TL;DR: The present article aims to provide a clear-cut picture of the current knowledge on the molecular nature and the role played by the components of the Ca(2+) machinery in vascular ECs under both physiological and pathological conditions.
OtherDOI

Transient Receptor Potential Channels and Endothelial Cell Calcium Signaling

TL;DR: In this review, an in-depth discussion of Ca2+ -permeable TRP channels in the endothelium and their role in vascular regulation is provided.
Journal ArticleDOI

Contribution of TRPC3 to store-operated calcium entry and inflammatory transductions in primary nociceptors

TL;DR: The findings highlight a major contribution of TRPC3 to neuronal calcium homeostasis in somatosensory pathways based on the unique ability of these cation channels to engage in both SOCE and receptor-operated calcium influx.
References
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Flow-mediated endothelial mechanotransduction

TL;DR: The transmission of hemodynamic forces throughout the endothelium and the mechanotransduction mechanisms that lead to biophysical, biochemical, and gene regulatory responses of endothelial cells to hemodynamic shear stresses are reviewed.
Journal ArticleDOI

Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells

TL;DR: PC1 and PC2 contribute to fluid-flow sensation by the primary cilium in renal epithelium and that they both function in the same mechanotransduction pathway, suggesting loss or dysfunction of PC1 or PC2 may lead to polycystic kidney disease.
Journal ArticleDOI

Ion channels and their functional role in vascular endothelium.

TL;DR: Evidence is presented for the involvement of ion channels in endothelial cell functions controlled by intracellular Ca(2+) signals, such as the production and release of many vasoactive factors, e.g., nitric oxide and PGI(2).
Journal ArticleDOI

Lack of an endothelial store-operated Ca2+ current impairs agonist-dependent vasorelaxation in TRP4-/- mice.

TL;DR: A store-operated Ca2+ current is described in vascular endothelium and it is shown that endothelial cells of mice deficient in TRP4 (also known as CCE1) lack this current, showing that TRP 4 is an indispensable component of store- operated channels in native endothelial Cells and that these channels directly provide an Ca2-entry pathway essentially contributing to the regulation of blood vessel tone.
Journal ArticleDOI

Flow activates an endothelial potassium channel to release an endogenous nitrovasodilator.

TL;DR: The data suggest that transmission of a hyperpolarizing current from endothelium to the vascular smooth muscle is not necessary for flow-mediated vasodilation, and that activation of this channel leads to the release of the endogenous nitrovasodilator, nitric oxide.
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