| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Institute of Pharmacology and Toxicology, University of Tuebingen, Tuebingen, Germany
2 Max-Planck-Institute for Experimental Endocrinology, Hannover, Germany
3 Institute of Pharmacology and Toxicology, University of Tuebingen, Tuebingen, Germany; Department of Medicine and Pharmacology, University of California San Diego, San Diego, USA
* To whom correspondence should be addressed. E-mail: vvallon{at}ucsd.edu.
In mouse kidney, the classical protein kinase C (PKC) isoenzyme alpha is expressed in glomeruli, cortical collecting duct (intercalated cells only) and medullary collecting duct. To get insights on its function, PKC alpha knockout (-/-) and wild type (+/+) mice were studied. When provided free access to water, PKC alpha -/- mice showed about 50% greater urine flow rate and lower urine osmolality in 24h metabolic cage experiments despite a greater urinary vasopressin to creatinine ratio versus PKC alpha +/+ mice. Renal albumin excretion was not different. Clearance experiments under inactin/ketamine anesthesia revealed a modestly reduced GFR and showed a reduced absolute and fractional renal fluid reabsorption in PKC alpha -/- mice. The sodium restricting response to a low sodium diet was unaffected in PKC alpha -/- mice. Urinary osmolality was reduced to similar hypotonic levels in PKC alpha -/- and +/+ mice during acute oral water loading or application of the vasopressin V2 receptor antagonist SR121463. In comparison, the lower urinary osmolality observed in PKC alpha -/- mice vs. wild type mice under basal conditions persisted during water restriction for 36h. In conclusion, PKC alpha appears not to play a major role in renal sodium reabsorption but consistent with its expression in medullary collecting duct contributes to urinary concentration in mice. Considering that PKC beta I and II are coexpressed with PKC alpha in mouse medullary collecting duct, the present results indicate that classical PKC isoenzymes cannot fully compensate for each other.
This article has been cited by other articles:
|
|
 |
|
  T. Rieg, K. Pothula, J. Schroth, J. Satriano, H. Osswald, J. Schnermann, P. A. Insel, R. A. Bundey, and V. Vallon Vasopressin regulation of inner medullary collecting ducts and compensatory changes in mice lacking adenosine A1 receptors Am J Physiol Renal Physiol, March 1, 2008; 294(3): F638 - F644. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. A. Fenton and M. A. Knepper Mouse Models and the Urinary Concentrating Mechanism in the New Millennium Physiol Rev, October 1, 2007; 87(4): 1083 - 1112. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W.-Y. Kim, J.-H. Jung, E.-Y. Park, C.-W. Yang, H. Kim, S. Nielsen, K. M. Madsen, and J. Kim Expression of protein kinase C isoenzymes {alpha}, betaI, and {delta} in subtypes of intercalated cells of mouse kidney Am J Physiol Renal Physiol, November 1, 2006; 291(5): F1052 - F1060. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Rieg, H. Steigele, J. Schnermann, K. Richter, H. Osswald, and V. Vallon Requirement of Intact Adenosine A1 Receptors for the Diuretic and Natriuretic Action of the Methylxanthines Theophylline and Caffeine J. Pharmacol. Exp. Ther., April 1, 2005; 313(1): 403 - 409. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Redling, I. L. Pfaff, M. Leitges, and V. Vallon Immunolocalization of protein kinase C isoenzymes {alpha}, {beta}I, {beta}II, {delta}, and {varepsilon} in mouse kidney Am J Physiol Renal Physiol, August 1, 2004; 287(2): F289 - F298. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
