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Acta Physiologica 2012; Volume 204, Supplement 689
91st Annual Meeting of The German Physiological Society
3/22/2012-3/25/2012
Dresden, Germany


OSR1-SENSITIVE INTESTINAL NA+ TRANSPORT
Abstract number: O87

Fajol1 *A., Pasham1 V., Pathare1 G., Michael1 D., Rexhepaj1 R., Rotte1 A., Foller1 M., Lang1 F.

1University of Tbingen, Department of Physiology, Tbingen, Germany

The oxidative stress responsive kinase 1 (OSR1) contributes to WNK-(with no K) dependent regulation of renal tubular salt transport, renal salt excretion and blood pressure. Little is known, however, about a role of OSR1 in the regulation of intestinal salt transport. Major intestinal Na+ reabsorption mechanisms include the intestinal Na+/H+ exchanger (NHE) and colonic Na+ channel ENaC. The present study thus explored, whether OSR1 is expressed in intestinal and colonic epithelium and whether intestinal NHE and colonic ENaC activities are different in knockin mice carrying one allele of WNK-resistant OSR1 (osr+/KI) and wild type mice (osr+/+). OSR protein abundance in intestinal tissue was determined by Western blotting, cytosolic pH (pHi) in intestinal cells from 2',7'-bis-(2-carboxyethyl)-5-(and-6)-carboxyfluorescein (BCECF) fluorescence, Na+/H+ exchanger activity from the Na+-dependent realkalinization following an ammonium pulse, and colonic ENaC activity from amiloride-sensitive transepithelial current in Ussing chamber experiments. As a result, OSR1 protein was expressed in intestine of both osr+/KI mice and osr+/+ mice. Daily fecal Na+ excretion was lower and intestinal NHE activity as well as amiloride-sensitive apical Na+ channel activity were higher in osr+/KI mice than in osr+/+ mice. Serum osmolarity as well as serum ADH, serum aldosterone and serum corticosterone concentrations were similar in both genotypes. In conclusion, OSR1 expressed in intestinal tisse and partial WNK insensitivity of OSR1 leads to enhanced intestinal Na+/H+ exchanger activity as well as increased colonic amiloride-sensitive Na+ current.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 204, Supplement 689 :O87

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