| Autor: |
Kondapalli KC; Department of Physiology, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD, 21205, USA.; Department of Natural Sciences, University of Michigan-Dearborn, 4901 Evergreen Road, Dearborn, MI, 48128, USA., Todd Alexander R; Division of Nephrology, Department of Pediatrics, University of Alberta, 11405-87 Avenue, Edmonton, AB, T6G 1C9, Canada., Pluznick JL; Department of Physiology, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD, 21205, USA., Rao R; Department of Physiology, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD, 21205, USA. rrao@jhmi.edu. |
| Abstrakt: |
Increased renal reabsorption of sodium is a significant risk factor in hypertension. An established clinical marker for essential hypertension is elevated sodium lithium countertransport (SLC) activity. NHA2 is a newly identified Na + (Li + )/H + antiporter with potential genetic links to hypertension, which has been shown to mediate SLC activity and H + -coupled Na + (Li + ) efflux in kidney-derived MDCK cells. To evaluate a putative role in sodium homeostasis, we determined the effect of dietary salt on NHA2. In murine kidney sections, NHA2 localized apically to distal convoluted (both DCT1 and 2) and connecting tubules, partially overlapping in distribution with V-ATPase, AQP2, and NCC1 transporters. Mice fed a diet high in sodium chloride showed elevated transcripts and expression of NHA2 protein. We propose a model in which NHA2 plays a dual role in salt reabsorption or secretion, depending on the coupling ion (sodium or protons). The identified novel regulation of Na + /H + antiporter in the kidney suggests new roles in salt homeostasis and disease. |
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