|
Hypertensive disease
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Potassium has recently been identified as an important driver of NCC activity, and low serum potassium may also contribute to increased renal sodium reabsorption and hypertension in CS.
|
29726949 |
2018 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Loss of physiological regulation of the renal thiazide-sensitive Na+-Cl- cotransporter (NCC) by mutant WNK1 or WNK4 results in pseudohypoaldosteronism type II (PHAII) characterized by arterial hypertension and hyperkalemia.
|
18701621 |
2008 |
|
Hypertensive disease
|
0.400 |
AlteredExpression
|
group |
BEFREE |
The thiazide-sensitive Na-Cl cotransporter (TSC) is involved in the fine regulation of sodium excretion by the kidney, and an increase in its activity causes salt-sensitive hypertension and hypercalciuria.
|
17885550 |
2007 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
There is emerging evidence that NCC, involved in hypertensive diseases, is also regulated by ubiquitylation.
|
24382868 |
2014 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
The aim of this review is to provide an overview of the recent developments in the regulation of NCC, highlighting a potential new therapeutic target for the treatment of hypertension.
|
21088576 |
2011 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
The increased expression of L-WNK1 in the DCT results in increased activity of the Na-Cl cotransporter (NCC) and thus hypervolemia and hypertension.
|
22080857 |
2012 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
CTD_human |
Upregulation of apical sodium-chloride cotransporter and basolateral chloride channels is responsible for the maintenance of salt-sensitive hypertension.
|
18480177 |
2008 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
These data exclude a primary role of the TSC gene in hypertension pathogenesis in the hypertension cohorts studied.
|
11564973 |
2001 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
In particular, CD8<sup>+</sup> T cells directly contact the distal convoluted tubule (DCT) in the kidneys of DOCA-salt mice and CD8<sup>+</sup> T cell-injected mice, leading to up-regulation of the Na-Cl co-transporter NCC, p-NCC and the development of salt-sensitive hypertension.
|
28067240 |
2017 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Here we tested whether STK39, OXSR1, and SLC12A3 genetically contribute to hypertension in the Han Chinese population and how the SNP to SNP or SNP to other risk factors interacts in the pathogenesis of hypertension.
|
20889219 |
2012 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Increased urinary Na-Cl cotransporter protein in familial hyperkalaemia and hypertension.
|
17951312 |
2008 |
|
Hypertensive disease
|
0.400 |
AlteredExpression
|
group |
BEFREE |
Taken together, these results demonstrate that loss of NEDD4-2 in adult renal tubules causes a new form of mild, salt-sensitive hypertension without hyperkalemia that is characterized by upregulation of NCC, elevation of β/γENaC, but not αENaC, and a normal Na+/K+ balance maintained by downregulation of ENaC activity and upregulation of ROMK.
|
23348737 |
2013 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Taken together, our findings demonstrate a predominant role played by SLC12A3 gene rs5804 in determining hypertension risk among northeastern Han Chinese.
|
24430698 |
2014 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
LHGDN |
Association study of variants in two ion-channel genes (TSC and CLCNKB) and hypertension in two ethnic groups in Northwest China.
|
17997379 |
2008 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Lack of association of variants of the renal salt reabsorption-related genes SLC12A3 and ClC-Kb and hypertension in Mongolian and Han populations in Inner Mongolia.
|
21644212 |
2011 |
|
Hypertensive disease
|
0.400 |
AlteredExpression
|
group |
BEFREE |
The pathophysiological significance of this network is illustrated by the fact that modification of each individual protein in the network changes NCC activity and results in salt-dependent hypotension or hypertension.
|
24310820 |
2014 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Association of TSC and WNK1 with hypertension was not observed.
|
15309683 |
2004 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
Low intracellular chloride stimulates WNK kinases to activate NCC, limiting potassium losses, even at the expense of increased blood pressure.
|
25565204 |
2015 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
In 2011 Fujita and coworkers proposed that beta-adrenergic stimulation causes decreased serine/threonine-protein kinase WNK4 transcription leading to the activation of Na-Cl cotransporter (NCC) which participates in salt sensitivity and salt hypertension development in rodents.
|
31647304 |
2019 |
|
Hypertensive disease
|
0.400 |
Biomarker
|
group |
BEFREE |
These findings suggest that NCC-mediated Cl<sup>-</sup> uptake plays important roles in the development of aldosterone-induced hypertension and renal injury.
|
29631358 |
2018 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
Mineralocorticoid synthesis and degradation, the mineralocorticoid receptor, sodium channel resorptive mechanisms, and regulation of the thiazide-sensitive sodium-chloride cotransporter have been shown to cause hypertension.
|
14871048 |
2004 |
|
Hypertensive disease
|
0.400 |
PosttranslationalModification
|
group |
BEFREE |
Metformin increased urinary sodium excretion by reducing phosphorylation of NCC, suggesting its role in improving hypertension.
|
29510178 |
2018 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
CA-SPAK mice displayed thiazide-treatable hypertension and hyperkalemia, concurrent with NCC hyperphosphorylation.
|
28442491 |
2017 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
We therefore studied microsatellite markers close to the thiazide-sensitive Na-Cl cotransporter on chromosome 16 and a quantitative trait locus for abdominal obesity-metabolic syndrome (AOMS2) on chromosome 17, which have been found to be linked to hypertension in a previous genome scan in Chinese.
|
15716982 |
2005 |
|
Hypertensive disease
|
0.400 |
GeneticVariation
|
group |
BEFREE |
FHHt (familial hyperkalaemic hypertension; also known as Gordon's syndrome) is a salt-dependent form of hypertension caused by mutations in the regulators of the thiazide-sensitive Na+-Cl- co-transporter NCC [also known as SLC12A3 (solute carrier family 12 member 3)] and is effectively treated by thiazide diuretics and/or dietary salt restriction.
|
24266877 |
2014 |