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• W2008348834 abstract "TRPV5 and TRPV6 channels are expressed in distal renal tubules and play important roles in the transcellular Ca2 + reabsorption in kidney. They are regulated by multiple intracellular factors including protein kinases A and C, membrane phospholipid PIP2, protons, and divalent ions Ca2 + and Mg2 +. Here, we report that fluid flow that generates shear force within the physiological range of distal tubular fluid flow activated TRPV5 and TRPV6 channels expressed in HEK cells. Flow-induced activation of channel activity was reversible and did not desensitize over 2 min. Fluid flow stimulated TRPV5 and 6-mediated Ca2 + entry and increased intracellular Ca2 + concentration. N-glycosylation-deficient TRPV5 channel was relatively insensitive to fluid flow. In cells coexpressing TRPV5 (or TRPV6) and Slo1-encoded maxi-K channels, fluid flow induced membrane hyperpolarization, which could be prevented by the maxi-K blocker iberiotoxin or TRPV5 and 6 blocker La3 +. In contrast, fluid flow did not cause membrane hyperpolarization in cells coexpressing ROMK1 and TRPV5 or 6 channel. These results reveal a new mechanism for the regulation of TRPV5 and TRPV6 channels. Activation of TRPV5 and TRPV6 by fluid flow may play a role in the regulation of flow-stimulated K+ secretion via maxi-K channels in distal renal tubules and in the mechanism of pathogenesis of thiazide-induced hypocalciuria." @default.
• W2008348834 created "2016-06-24" @default.
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• W2008348834 date "2013-12-01" @default.
• W2008348834 modified "2023-10-15" @default.
• W2008348834 title "Flow-induced activation of TRPV5 and TRPV6 channels stimulates Ca2+-activated K+ channel causing membrane hyperpolarization" @default.
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• W2008348834 doi "https://doi.org/10.1016/j.bbamcr.2013.08.017" @default.
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