Submitted on March 24, 2007
Accepted on September 11, 2007
Adaptive redistribution of NBCe1-A and NBCe1-B in rat kidney proximal tubule and striated ducts of salivary glands during acid-base disturbances
Alena Brandes1, Oliver Oehlke1, Anne Schumann1, Stefanie Heidrich1, Frank Thevenod2, and Eleni Roussa3*
1 Center for Anatomy, Department of Neuroanatomy, University of Goettingen, Goettingen, Germany
2 Physiology & Pathophysiology, University of Witten/Herdecke, Faculty of Medicine, Witten, Germany
3 Univ Gottingen, United States; Univ Gottingen
* To whom correspondence should be addressed. E-mail: eroussa{at}gwdg.de.
The cellular distribution of the NH2-terminal NBCe1 variants NBCe1-A and NBCe1-B has been investigated in rat kidney and submandibular gland (SMG) under physiological conditions and after systemic acid-base perturbations. Moreover, the in vivo data were complemented in vitro using the rat kidney proximal tubule (PT) cell line WKPT-0293 Cl.2. NBCe1-A was basolaterally localized in PT cells, whereas NBCe1-B exhibited intracellular and basolateral distribution. SMG showed transcript and protein expression for NBCe1-A and NBCe1 B. NBCe1-B was basolaterally localized in duct cells, NBCe1-A was found intracellularly in salivary striated ducts and apically in main duct cells. Acute metabolic acidosis significantly increased cells showing basolateral NBCe1-A in the PT indicating increased HCO3- reabsorption and significantly decreased cells exhibiting basolateral NBCe1-B in the salivary ducts suggesting decreased HCO3- secretion. Chronic acidosis had no effect on NBCe1 distribution in PT but significantly increased cells with basolateral NBCe1-A in salivary striated duct cells suggesting increased HCO3- reabsorption. In contrast, chronic alkalosis caused adaptive redistribution of NBCe1-A and NBCe1-B in renal PT favoring decreased HCO3- reabsorption. In vitro, WKPT-0293 Cl.2 cells expressed key acid-base transporters. Extracellular alkalosis down-regulated NBCe1-A protein. WKPT-0293 Cl.2 cells are therefore a useful model to study renal acid-base regulation in vitro. The results propose redistribution of the transporters as a potential post-translational regulation modus during acid-base disturbances. Moreover, the data demonstrate that renal PT and salivary duct epithelia respond to acid-base disturbances by an opposite redistribution pattern for NBCe1-A and NBCe1-B, reflecting specialized functions as HCO3- -reabsorbing and HCO3- -secreting epithelium, respectively.
