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• W2061529535 abstract "The largest peripheral blood pressure drop occurs in terminal arterioles (<40 µm lumen diameter). L-type voltage-dependent Ca 2+ channels (VDCCs) are considered the primary pathway for Ca 2+ influx during physiologic activation of vascular smooth muscle cells (VSMC). Recent evidence suggests that T-type VDCCs are expressed in renal afferent and efferent arterioles, mesenteric arterioles, and skeletal muscle arterioles. T-type channels are small-conductance, low voltage-activated, fast-inactivating channels. Thus, their role in supplying Ca 2+ for contraction of VSMC has been disputed. However, T-type channels display non-inactivating window currents, which may play a role in sustained Ca 2+ entry. Here, we review the possible role of T-type channels in vasomotor tone regulation in rat mesenteric terminal arterioles. The Ca V 3.1 channel was immunolocalized in VSMC, whereas the Ca V 3.2 channel was predominantly expressed in endothelial cells. Voltage-dependent Ca 2+ entry was inhibited by the new specific T-type blockers R(–)-efonidipine and NNC 55-0396. The effect of NNC 55-0396 persisted in depolarized arterioles, suggesting an unusually high activation threshold of mesenteric T-type channels. T-type channels were not necessary for conduction of vasoconstriction, but appear to be important for local electromechanical coupling in VSMC. The first direct demonstration of endothelial T-type channels warrants new investigations of their role in vascular biology." @default.
• W2061529535 created "2016-06-24" @default.
• W2061529535 creator A5015097155 @default.
• W2061529535 creator A5052648487 @default.
• W2061529535 date "2009-01-01" @default.
• W2061529535 modified "2023-09-25" @default.
• W2061529535 title "Is there a role for T-type Ca²⁺ channels in regulation of vasomotor tone in mesenteric arterioles?This article is part of a Special Issue on Information Transfer in the Microcirculation." @default.
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• W2061529535 doi "https://doi.org/10.1139/y08-101" @default.
• W2061529535 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19142211" @default.
• W2061529535 hasPublicationYear "2009" @default.
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