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Departments of 1 Molecular Genetics, Biochemistry, and Microbiology and 2 Molecular and Cellular Physiology, The University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0524; and 3 Department of Biological Sciences, Northern Kentucky University, Highland Heights, Kentucky 41099
The degree to which loss of the
NHE3 Na+/H+ exchanger in the kidney contributes
to impaired Na+-fluid volume homeostasis in NHE3-deficient
(Nhe3
/) mice is unclear because of the
coexisting intestinal absorptive defect. To more accurately assess the
renal effects of NHE3 ablation, we developed a mouse with transgenic
expression of rat NHE3 in the intestine and crossed it with
Nhe3/ mice. Transgenic
Nhe3/ (tgNhe3/)
mice tolerated dietary NaCl depletion better than nontransgenic knockouts and showed no evidence of renal salt wasting. Unlike nontransgenic Nhe3/ mice,
tgNhe3/ mice tolerated a 5% NaCl diet. When
fed a 5% NaCl diet, tgNhe3/ mice had lower
serum aldosterone than tgNhe3/ mice on a 1%
NaCl diet, indicating improved extracellular fluid volume status.
Na+-loaded tgNhe3/ mice had
sharply increased urinary Na+ excretion, reflective of
increased absorption of Na+ in the small intestine;
nevertheless, they remained hypotensive, and renal studies showed a
reduction in glomerular filtration rate (GFR) similar to that observed
in nontransgenic Nhe3/ mice. These data show
that reduced GFR, rather than being secondary to systemic hypovolemia,
is a major renal compensatory mechanism for the loss of NHE3 and
indicate that loss of NHE3 in the kidney alters the set point for
Na+-fluid volume homeostasis.
sodium/hydrogen exchanger; diarrhea; Slc9a3; sodium absorption; sodium-fluid volume homeostasis
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