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TRPV4 as a flow sensor in flow-dependent K⁺ secretion from the cortical collecting duct

Divisions of ¹Molecular Pharmacology and ²Clinical Pharmacology, Department of Pharmacology, Jichi Medical University, Tochigi, Japan

Submitted 21 November 2005 ; accepted in final form 30 August 2006

The transient receptor vanilloid-4 (TRPV4) is a mechanosensitive, swell-activated cation channel that is abundant in the renal distal tubules. Immunolocalization studies, however, present conflicting data as to whether TRPV4 is expressed along the apical and/or basolateral membranes. To disclose the role of TRPV4 in flow-dependent K⁺ secretion in distal tubules in vivo, urinary K⁺ excretion and net transports of K⁺ and Na⁺ in the cortical collecting duct (CCD) were measured with an in vitro microperfusion technique in TRPV4^+/+ and TRPV4^–/– mice. Both net K⁺ secretion and Na⁺ reabsorption were flow dependently increased in the CCDs isolated from TRPV4^+/+mice, which were significantly enhanced by a luminal application of 50 µM 4-phorbol-12,13-didecanoate (4PDD), an agonist of TRPV4. No flow dependence of net K⁺ and Na⁺ transports or effects of 4PDD on CCDs were observed in TRPV4^–/– mice. A basolateral application of 4PDD had little effect on these ion transports in the TRPV4^+/+ CCDs, while the luminal application did. Urinary K⁺ excretion was significantly smaller in TRPV4^–/– than in TRPV4^+/+ mice when urine production was stimulated by a venous application of furosemide. These observations suggested an essential role of the TRPV4 channels in the luminal or basolateral membrane as flow sensors in the mechanism underlying the flow-dependent K⁺ secretion in mouse CCDs.

shear stress; mechanoreceptor; K⁺ excretion; maxi-K⁺ channel

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