JPET xPharm- The Comprehensive Pharmacology Reference

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
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 Proksch, J. W.
Right arrow Articles by Mayeux, P. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Proksch, J. W.
Right arrow Articles by Mayeux, P. R.

Effects of lipid A on calcium homeostasis in renal proximal tubules

JW Proksch, LA Traylor and PR Mayeux

Department of Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, USA.

It is clear that lipopolysaccharides (LPS) are responsible for the multiorgan failure often associated with endotoxemia. However, little is known of the direct effects of LPS on kidney cells. We examined the effects of lipid A, the biologically active component of LPS, on rat proximal tubule Ca++ homeostasis. Lipid A produced a rapid, transient, concentration-dependent rise in intracellular Ca++ concentration, [Ca++]i, as monitored by fura-2. At 50 micrograms/ml [Ca++]i rose to 138 +/- 12 nM (n = 4) above basal [Ca++]i levels. The response to lipid A was not significantly inhibited by chelating extracellular Ca++ with EGTA (5 mM). However, the rise in [Ca++]i was significantly inhibited by 8-(N,N-dimethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride) and thapsigargin (17 +/- 7 nM and 13 +/- 9 nM rise, respectively; P < .05). These data indicate that the rise in [Ca++]i induced by lipid A is due to release of intracellular stores, and not extracellular influx. We also examined the role of inositol 1,4,5-trisphosphate in the lipid A response. Lipid A caused a time-dependent increase in inositol 1,4,5-trisphosphate that paralleled the rise in [Ca++]i, suggesting the release in [Ca++]i is through an inositol 1,4,5- trisphosphate-mediated release of intracellular stores. The ability of lipid A to alter Ca++ homeostasis suggests a potential for LPS to directly alter proximal tubule physiology and renal function in vivo.

Volume 276, Issue 2, pp. 555-560, 02/01/1996
Copyright © 1996 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
 J DAIRY SCIHome page
M. R. Waldron, B. J. Nonnecke, T. Nishida, R. L. Horst, and T. R. Overton
Effect of Lipopolysaccharide Infusion on Serum Macromineral and Vitamin D Concentrations in Dairy Cows
J Dairy Sci, November 1, 2003; 86(11): 3440 - 3446.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
C. Zhang and P. R. Mayeux
NO/cGMP signaling modulates regulation of Na+-K+-ATPase activity by angiotensin II in rat proximal tubules
Am J Physiol Renal Physiol, March 1, 2001; 280(3): F474 - F479.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1996 by the American Society for Pharmacology and Experimental Therapeutics.