AJP - Renal AJP: Lung Cellular and Molecular Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Am J Physiol Renal Physiol (August 5, 2003). doi:10.1152/ajprenal.00198.2003
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
285/6/F1100    most recent
00198.2003v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Asghar, M.
Right arrow Articles by Lokhandwala, M. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Asghar, M.
Right arrow Articles by Lokhandwala, M. F.
Submitted on May 27, 2003
Accepted on July 30, 2003

Over-expression of PKC-{beta}I and -{delta} contributes to higher PKC activity in the proximal tubules of old Fischer 344 rats

Mohammad Asghar1, Tahir Hussain1, and Mustafa F. Lokhandwala1*

1 Heart and Kidney Institute, College of Pharmacy, University of Houston, Houston, TX, USA

* To whom correspondence should be addressed. E-mail: MLOKHANDWALA{at}UH.EDU.

Previously, we have reported that natriuretic and diuretic response to dopamine is diminished in old Fischer 344 rats which is due to higher basal protein kinase C (PKC) activity and hyper-phosphorylation of Na,K-ATPase in the proximal tubules (PTs) of old rats. The present study was conducted to determine whether higher PKC activity could be due to altered expression of some of the PKC isoforms in the superficial cortex (rich in PTs) of old rats. Fluorimetric measurement showed almost two-fold increase in the PKC activities in homogenates and membranes of old (24-month) compared to adult (6-month) rats. Interestingly, in the basal state PKC-{beta}I was over-expressed in the membranes while PKC-{delta} expression was increased in the cytosol of old compared to adult rats. Treatment of the cortical slices with either SKF 38393, a D1-like agonist, or PDBu, a direct activator of PKC caused translocation of PKC-{beta}I from cytosol to membranes in adult but not in old rats. Both these drugs caused translocation of PKC-{delta} from membranes to cytosol in adult but not in old rats. These drugs had no effect on translocation of PKC-{zeta} in both adult and old rats. Both PKC-{beta}I and -{delta} co-immunoprecipiated with {alpha}1-subunit of Na,K-ATPase in adult and old rats. These observations suggest that both SKF 38393 and PDBu differentially regulate PKC-{beta}I and -{delta} in adult but not in old rats. Also, PKC-{beta}I and -{delta} seem to interact with Na,K-ATPase in these animals. The over-expression of both PKC-{beta}I and -{delta} in old rats could be responsible for a higher basal PKC activity, which causes the hyper-phosphorylation of Na,K-ATPase and contributes to the diminished inhibition of Na,K-ATPase activity by dopamine in old rats.




This article has been cited by other articles:


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
C. Zeng, I. Armando, Y. Luo, G. M. Eisner, R. A. Felder, and P. A. Jose
Dysregulation of dopamine-dependent mechanisms as a determinant of hypertension: studies in dopamine receptor knockout mice
Am J Physiol Heart Circ Physiol, February 1, 2008; 294(2): H551 - H569.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
A. A. Banday, F. R. Fazili, and M. F. Lokhandwala
Insulin causes renal dopamine D1 receptor desensitization via GRK2-mediated receptor phosphorylation involving phosphatidylinositol 3-kinase and protein kinase C
Am J Physiol Renal Physiol, September 1, 2007; 293(3): F877 - F884.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
A. A. Banday and M. F. Lokhandwala
Oxidative stress reduces renal dopamine D1 receptor-Gq/11{alpha} G protein-phospholipase C signaling involving G protein-coupled receptor kinase 2
Am J Physiol Renal Physiol, July 1, 2007; 293(1): F306 - F315.
[Abstract] [Full Text] [PDF]


Home page
J. Am. Soc. Nephrol.Home page
A. A. Banday, F. R. Fazili, and M. F. Lokhandwala
Oxidative Stress Causes Renal Dopamine D1 Receptor Dysfunction and Hypertension via Mechanisms That Involve Nuclear Factor-{kappa}B and Protein Kinase C
J. Am. Soc. Nephrol., May 1, 2007; 18(5): 1446 - 1457.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
R. Z. Fardoun, M. Asghar, and M. Lokhandwala
Role of oxidative stress in defective renal dopamine D1 receptor-G protein coupling and function in old Fischer 344 rats
Am J Physiol Renal Physiol, November 1, 2006; 291(5): F945 - F951.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Renal Physiol.Home page
A. Marwaha and M. F. Lokhandwala
Tempol reduces oxidative stress and restores renal dopamine D1-like receptor- G protein coupling and function in hyperglycemic rats
Am J Physiol Renal Physiol, July 1, 2006; 291(1): F58 - F66.
[Abstract] [Full Text] [PDF]


Home page
Physiol. GenomicsHome page
C. Zeng, H. Sanada, H. Watanabe, G. M. Eisner, R. A. Felder, and P. A. Jose
Functional genomics of the dopaminergic system in hypertension
Physiol Genomics, November 17, 2004; 19(3): 233 - 246.
[Abstract] [Full Text] [PDF]


Home page
Exp. Biol. Med.Home page
M. Asghar and M. F. Lokhandwala
Antioxidant Supplementation Normalizes Elevated Protein Kinase C Activity in the Proximal Tubules of Old Rats
Experimental Biology and Medicine, March 1, 2004; 229(3): 270 - 275.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1976 by the American Physiological Society.