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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 4α-phorbol-12,13-didecanoate (4αPDD), an agonist of TRPV4. No flow dependence of net K +  and Na +  transports or effects of 4αPDD on CCDs were observed in TRPV4  −/−  mice. A basolateral application of 4αPDD 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.

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

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