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lüll TRPV4 as a flow sensor in flow-dependent K+ secretion from the cortical collecting duct Taniguchi J; Tsuruoka S; Mizuno A; Sato J; Fujimura A; Suzuki MAm J Physiol Renal Physiol 2007[Feb]; 292 (2): F667-73The 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 microM 4alpha-phorbol-12,13-didecanoate (4alphaPDD), an agonist of TRPV4. No flow dependence of net K(+) and Na(+) transports or effects of 4alphaPDD on CCDs were observed in TRPV4(-/-) mice. A basolateral application of 4alphaPDD 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.|Amiloride/pharmacology[MESH]|Animals[MESH]|Charybdotoxin/pharmacology[MESH]|Desoxycorticosterone/pharmacology[MESH]|Furosemide/pharmacology[MESH]|In Vitro Techniques[MESH]|Kidney Tubules, Collecting/drug effects/*physiology[MESH]|Male[MESH]|Mice[MESH]|Phorbol Esters/pharmacology[MESH]|Potassium/*metabolism/urine[MESH]|TRPV Cation Channels/deficiency/*physiology[MESH] |