Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Editor

Personal info

View

About

Terms

Javascript disabled

Please enable Javascript support in your browser to use this application.

Instructions on how to enable JavaScript on different browsers can be found here: http://www.google.com/support/bin/answer.py?answer=23852.

[edit this page]

Paillard, M.

H+ and HCO3- transporters in the medullary thick ascending limb of the kidney: molecular mechanisms, function and regulation.

The H+ and HCO3- transporters present in the medullary thick ascending limb (MTAL) of the kidney are involved in several functions, such as transepithelial transport, defense of cell pH and cell volume. Apical H+ secretion occurs via the NHE-3 and NHE-2 isoforms of the Na+/H+ exchanger, and H(+)-ATPase. The apical Na+/H+ exchanger is responsible for most of the apical step of transepithelial HCO3- absorption and is unresponsive to cell acidification under isosmotic conditions. Basolateral HCO3- efflux mechanisms may occur via the Cl-/HCO3- exchanger and via the cotransporters K+/HCO3- (in the rat) and Na-3HCO3- (in the mouse). However, the role of each transporter in transepithelial HCO3- absorption is currently unknown. Inhibition of the basolateral Na+/H+ exchanger ( NHE-1) paradoxically inhibits the apical Na+/H+ exchanger. This cross talk is independent of cell pH and may involve variations in cell volume. Arginine vasopressin ( AVP) and hyperosmolality induce a differential regulation of basolateral NHE-1 and the apical Na+/H+ exchanger. They stimulate the basolateral NHE-1, and the resulting cell alkalinization probably stimulates the pHi-sensitive AE2, which restores cell volume by cellular uptake of NaCl. They also inhibit the apical Na+/H+ exchanger, which reduces net HCO3- absorption and thus may prevent interstitial fluid alkalinization. Chronic metabolic acidosis markedly increases HCO3- absorptive capacity of MTAL, by stimulating at least the synthesis of apical NHE-3 protein, as in the proximal tubule. Conversely, chronic metabolic alkalosis reduces the apical NHE-3 transport activity by decreasing the synthesis of NHE-3 protein. The paradoxical increase in HCO3- absorptive capacity of MTAL observed in the model of chronic NaHCO3-load alkalosis should be due to other factors overcoming the inhibitory effect of alkalosis on NHE-3.[1]

References

H+ and HCO3- transporters in the medullary thick ascending limb of the kidney: molecular mechanisms, function and regulation. Paillard, M. Kidney Int. Suppl. (1998) [Pubmed]

Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenes Open Access Licence Privacy Policy Terms of Use apsburg

The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.