| First Author | Vallon V | Year | 2001 |
| Journal | J Am Soc Nephrol | Volume | 12 |
| Issue | 10 | Pages | 2003-11 |
| PubMed ID | 11562398 | Mgi Jnum | J:103378 |
| Mgi Id | MGI:3609300 | Doi | 10.1681/ASN.V12102003 |
| Citation | Vallon V, et al. (2001) Role of KCNE1-dependent K+ fluxes in mouse proximal tubule. J Am Soc Nephrol 12(10):2003-11 |
| abstractText | The electrochemical gradient for K+ across the luminal membrane of the proximal tubule favors K+ fluxes to the lumen. Here it was demonstrated by immunohistochemistry that KCNE1 and KCNQ1, which form together the slowly activated component of the delayed rectifying K+ current in the heart, also colocalize in the luminal membrane of proximal tubule in mouse kidney. Micropuncture experiments revealed a reduced K+ concentration in late proximal and early distal tubular fluid as well as a reduced K+ delivery to these sites in KCNE1 knockout (-/-), compared with wild-type (+/+) mice. These observations would be consistent with KCNE1-dependent K+ fluxes to the lumen in proximal tubule. Electrophysiological studies in isolated perfused proximal tubules indicated that this K+ flux is essential to counteract membrane depolarization due to electrogenic Na+-coupled transport of glucose or amino acids. Clearance studies revealed an enhanced fractional urinary excretion of fluid, Na+, Cl-, and glucose in KCNE1 -/- compared with KCNE1 +/+ mice that may relate to an attenuated transport in proximal tubule and contribute to volume depletion in these mice, as indicated by higher hematocrit values. |
