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1 Molecular Pharmacology, Jichi Medical school, Japan
2 Molecular Pharmacology, Jichi Medical school, Kawachi, Tochigi, Japan; Clinical pharmacology, Jichi Medical school, Kawachi, Tochigi, Japan
* To whom correspondence should be addressed. E-mail: macsuz{at}jichi.ac.jp.
The transient receptor vanilloid 4 (TRPV4) is a mechano-sensitive, 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, urinary K+ excretion in vivo and net transports of K+ and Na+ in the cortical collecting duct (CCD) with an in vitro microperfusion technique were measured 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 effects 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.
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