| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 UMR7134, CNRS-UPMC, Paris, France
2 U773, INSERM, Paris, France
3 Department of Pharmacology, Graduate School of Medicine, Osaka, Japan
4 Department of Pharmacology, Graduate School of Medicie, Osaka, Japan
* To whom correspondence should be addressed. E-mail: Marc.Paulais{at}bhdc.jussieu.fr.
K+ channels in the basolateral membrane of mouse cortical collecting duct (CCD) principal cells were identified using the patch-clamp technique, real time PCR and immunohistochemistry. In cell-attached membrane patches, three K+ channels with conductances of ~ 75, 40 and 20 pS were observed, but the K+ channel with the intermediate conductance (40 pS) predominated. In inside-out membrane patches exposed to an Mg2+-free medium, the current-voltage relationship of the intermediate conductance channel was linear with a conductance of 38 pS. Adding 1.3 mM internal Mg2+ had no influence on the inward conductance (Gin = 35 pS), but reduced outward conductance (Gout) to 13 pS, yielding a Gin/Gout of 3.2. The polycation spermine (6x10-7 M) reduced its activity on inside-out membrane patches by 50 % at Vc = 60 mV. Channel activity was also dependent on intracellular pH (pHi) : a sigmoid relationship between pHi and channel NPo was observed with a pK of 7.24 and a Hill coefficient of 1.7. By real-time PCR on CCD extracts, Kir4.1 and Kir5.1, but not Kir4.2, mRNAs were detected. Kir4.1 and Kir5.1 proteins cellularly co-localized with AQP2, a specific marker of CCD principal cells, while AQP2-negative cells (i.e. intercalated cells) showed no staining. Dietary K+ had no influence on the properties of the intermediate conductance channel, but a Na+-depleted diet increased its open probability by ~ 25 %. We conclude that Kir4.1/Kir5.1 channel is a major component of the K+ conductance in the basolateral membrane of mouse CCD principal cells.
This article has been cited by other articles:
|
|
 |
|
  L. M. Lewis, G. Bhave, B. A. Chauder, S. Banerjee, K. A. Lornsen, R. Redha, K. Fallen, C. W. Lindsley, C. D. Weaver, and J. S. Denton High-Throughput Screening Reveals a Small-Molecule Inhibitor of the Renal Outer Medullary Potassium Channel and Kir7.1 Mol. Pharmacol., November 1, 2009; 76(5): 1094 - 1103. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Sindic, C. Huang, A.-P. Chen, Y. Ding, W. A. Miller-Little, D. Che, M. F. Romero, and R. T. Miller MUPP1 complexes renal K+ channels to alter cell surface expression and whole cell currents Am J Physiol Renal Physiol, July 1, 2009; 297(1): F36 - F45. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. I. Scholl, M. Choi, T. Liu, V. T. Ramaekers, M. G. Hausler, J. Grimmer, S. W. Tobe, A. Farhi, C. Nelson-Williams, and R. P. Lifton Seizures, sensorineural deafness, ataxia, mental retardation, and electrolyte imbalance (SeSAME syndrome) caused by mutations in KCNJ10 PNAS, April 7, 2009; 106(14): 5842 - 5847. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
