HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/R1294    most recent 00261.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kanaan, A. Articles by Haddad, G. G. Search for Related Content PubMed PubMed Citation Articles by Kanaan, A. Articles by Haddad, G. G.

DEVELOPMENTAL PHYSIOLOGY AND PREGNANCY

Effect of chronic elevated carbon dioxide on the expression of acid-base transporters in the neonatal and adult mouse

Departments of ¹Pediatrics (Section of Respiratory Medicine) and ²Neuroscience, University of California San Diego, La Jolla; ³The Rady Children's Hospital, San Diego, California; ⁴Molecular Medicine and Renal Units, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts; ⁵Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut

Submitted 17 April 2007 ; accepted in final form 19 July 2007

Several pulmonary and neurological conditions, both in the newborn and adult, result in hypercapnia. This leads to disturbances in normal pH homeostasis. Most mammalian cells maintain tight control of intracellular pH (pH_i) using a group of transmembrane proteins that specialize in acid-base transport. These acid-base transporters are important in adjusting pH_i during acidosis arising from hypoventilation. We hypothesized that exposure to chronic hypercapnia induces changes in the expression of acid-base transporters. Neonatal and adult CD-1 mice were exposed to either 8% or 12% CO₂ for 2 wk. We used Western blot analysis of membrane protein fractions from heart, kidney, and various brain regions to study the response of specific acid-base transporters to CO₂. Chronic CO₂ increased the expression of the sodium hydrogen exchanger 1 (NHE1) and electroneutral sodium bicarbonate cotransporter (NBCn1) in the cerebral cortex, heart, and kidney of neonatal but not adult mice. CO₂ increased the expression of electrogenic NBC (NBCe1) in the neonatal but not the adult mouse heart and kidney. Hypercapnia decreased the expression of anion exchanger 3 (AE3) in both the neonatal and adult brain but increased AE3 expression in the neonatal heart. We conclude that: 1) chronic hypercapnia increases the expression of the acid extruders NHE1, NBCe1 and NBCn1 and decreases the expression of the acid loader AE3, possibly improving the capacity of the cell to maintain pH_i in the face of acidosis; and 2) the heterogeneous response of tissues to hypercapnia depends on the level of CO₂ and development.

anion exchanger; sodium bicarbonate cotransporter; sodium hydrogen exchanger; acidosis; hypercapnia

This article has been cited by other articles:

				J. L. Aschner and R. L. Poland Sodium Bicarbonate: Basically Useless Therapy Pediatrics, October 1, 2008; 122(4): 831 - 835. [Abstract] [Full Text] [PDF]