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1 Department of Medicine, University of Cincinnati School of Medicine, Cincinnati, Ohio, USA; Research Services, Veterans Affairs Medical Center, Cincinnati, Ohio, USA
2 Department of Medicine, University of Cincinnati School of Medicine, Cincinnati, Ohio, USA
3 Department of Medical Genetics and Division of Renal Medicine, University of Cambridge, Cambridge, United Kingdom
* To whom correspondence should be addressed. E-mail: snezana.petrovic{at}uc.edu.
SLC26A7 is a newly identified basolateral Cl-/HCO3- exchanger specific to A-intercalated cells of the outer medullary collecting duct (OMCD). The purpose of the current experiments was to examine the expression of SLC26A7 in kidneys of vasopressin-deficient Brattleboro rats, before and after treatment with dDAVP. Brattleboro rats were treated with dDAVP, a vasopressin analog, for eight days, and their kidneys were examined for the expression of SLC26A7. Surprisingly, the expression of SLC26A7 protein, as examined by immunofluorescence, was undetectable in kidneys of Brattleboro rats. However, treatment with dDAVP induced the expression of SLC26A7 protein in OMCD and restored it to the levels observed in normal rats. These results were verified by Western blot analysis. The mRNA expression of SLC26A7, however, remained unchanged in response to dDAVP. Immunofluorescent labeling of AE1 demonstrated abundant levels in OMCD of Brattleboro rats and a mild reduction in response to dDAVP. The abundance of H+-ATPase was not affected by dDAVP. The increased SLC26A7 expression correlated with enhanced AQP2 expression in outer medulla. In conclusion, vasopressin increases the membrane abundance of SLC26A7 through post-transcriptional mechanisms in OMCD. We suggest that the induction of SLC26A7 in kidneys of Brattleboro rats is an attempt by A-intercalated cells of OMCD to regulate their volume and pH and maintain bicarbonate absorption in response to vasopressin.
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