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PTH-independent regulation of blood calcium concentration by the calcium-sensing receptor.
Tight regulation of calcium levels is required for many critical biological functions. The Ca2+-sensing receptor (CaSR) expressed by parathyroid cells controls blood calcium concentration byExpand
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Common noncoding UMOD gene variants induce salt-sensitive hypertension and kidney damage by increasing uromodulin expression
Hypertension and chronic kidney disease (CKD) are complex traits representing major global health problems. Multiple genome-wide association studies have identified common variants in the promoter ofExpand
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Polyhydramnios, Transient Antenatal Bartter's Syndrome, and MAGED2 Mutations.
BACKGROUND Three pregnancies with male offspring in one family were complicated by severe polyhydramnios and prematurity. One fetus died; the other two had transient massive salt-wasting and polyuriaExpand
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Chronic metabolic acidosis enhances NHE-3 protein abundance and transport activity in the rat thick ascending limb by increasing NHE-3 mRNA.
Chronic metabolic acidosis (CMA) is associated with an adaptive increase in the bicarbonate absorptive capacity of the rat medullary thick ascending limb (MTAL). To specify whether NHE-3, the apicalExpand
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SPAK differentially mediates vasopressin effects on sodium cotransporters.
Activation of the Na(+)-K(+)-2Cl(-)-cotransporter (NKCC2) and the Na(+)-Cl(-)-cotransporter (NCC) by vasopressin includes their phosphorylation at defined, conserved N-terminal threonine and serineExpand
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RT-PCR analysis of Na+/H+ exchanger mRNAs in rat medullary thick ascending limb.
The thick ascending limb (TAL) of rat kidney absorbs bicarbonate secondary to proton secretion, but displays both basolateral and luminal Na+/H+ exchange (NHE) activity. Several NHE genes, includingExpand
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A Highly Conserved Motif at the COOH Terminus Dictates Endoplasmic Reticulum Exit and Cell Surface Expression of NKCC2*
Mutations in the apically located Na+-K+-2Cl− co-transporter, NKCC2, lead to type I Bartter syndrome, a life-threatening kidney disorder, yet the mechanisms underlying the regulation of mutated NKCC2Expand
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NKCC2 Surface Expression in Mammalian Cells
Apical bumetanide-sensitive Na+-K+-2Cl- co-transporter, termed NKCC2, is the major salt transport pathway in kidney thick ascending limb. NKCC2 surface expression is subject to regulation byExpand
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Endothelin-1/endothelin-B receptor-mediated increases in NHE3 activity in chronic metabolic acidosis.
Decreases in blood pH activate NHE3, the proximal tubular apical membrane Na/H antiporter. In cultured renal epithelial cells, activation of the endothelin-B (ET(B)) receptor increases NHE3 activity.Expand
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Expression of rat thick limb Na/H exchangers in potassium depletion and chronic metabolic acidosis.
BACKGROUND Regulation of renal transporter expression has been shown to support adaptation of transporter activities in several chronic situations. Basolateral and apical Na/H exchangers (NHE) inExpand
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