|
Hypertensive disease
|
0.300 |
Biomarker
|
group |
BEFREE |
In conclusion, NHE3 in the proximal tubules of the kidney may be a therapeutical target in hypertension induced by Ang II or with increased NHE3 expression in the proximal tubules.
|
31352824 |
2019 |
|
Hypertensive disease
|
0.300 |
Biomarker
|
group |
BEFREE |
Angiotensin III/AT<sub>2</sub> Receptor/NHE3 Signaling Pathway in the Proximal Tubules of the Kidney: A Novel Natriuretic and Antihypertensive Mechanism in Hypertension.
|
31039655 |
2019 |
|
Hypertensive disease
|
0.300 |
Biomarker
|
group |
BEFREE |
Nonmuscle myosin IIA and unconventional myosin VI move cargoes in anterograde and retrograde directions, respectively, and are known to redistribute along with NHE3 in the proximal tubule in response to a variety of natriuretic and antinatriuretic stimuli, including stimulation or inhibition of the renin-angiotensin system, high dietary Na<sup>+</sup> intake, and high blood pressure.
|
30864843 |
2019 |
|
Hypertensive disease
|
0.300 |
Biomarker
|
group |
BEFREE |
We hypothesize that NHE3 in the proximal tubules is necessary for maintaining basal blood pressure homeostasis and the development of ANG II-induced hypertension.
|
30849009 |
2019 |
|
Hypertensive disease
|
0.300 |
Biomarker
|
group |
BEFREE |
Since NHE3 promotes sodium absorption, and it was increased in HFD group, this finding could contribute to explain the hypertension observed in obesity.
|
29626530 |
2018 |
|
Hypertensive disease
|
0.300 |
Biomarker
|
group |
BEFREE |
The cytosolic calcium in the WKY or SHR rats was ~100 nM and was increased by ANG-(1-7) at 10<sup>-9</sup> or 10<sup>-6</sup> M. In hypertensive animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated the hypertension caused by the high plasma level of ANG II.
|
28490531 |
2017 |
|
Hypertensive disease
|
0.300 |
AlteredExpression
|
group |
BEFREE |
Taken together, our data suggest that fructose via uric acid stimulates renal expression of PRR/soluble PRR that stimulate sodium/hydrogen exchanger 3 and Na/K/2Cl cotransporter expression and intrarenal renin-angiotensin system to induce salt-sensitive hypertension.
|
27993957 |
2017 |
|
Hypertensive disease
|
0.300 |
AlteredExpression
|
group |
BEFREE |
Increased dietary fructose intake for several weeks upregulated the expression of NHE3, PAT1 and Glut5 in the intestine and resulted in hypertension in wild-type mice, a response that was almost abolished in PAT1 null mice and abrogated in Glut5 null mice.
|
21143427 |
2011 |
|
Hypertensive disease
|
0.300 |
AlteredExpression
|
group |
BEFREE |
The increase in renal proximal tubule ion transport in polygenic hypertension is primarily due to increased activity of NHE3 and Cl/HCO3 exchanger at the luminal/apical membrane and a primary or secondary increase in Na+/K+ATPase activity.
|
19654544 |
2009 |
|
Hypertensive disease
|
0.300 |
GeneticVariation
|
group |
BEFREE |
The objectives of this study were to identify polymorphic variants within the gene coding for the sodium/hydrogen exchanger type 3 (NHE3) and to examine their relationship with hypertension and biochemical indices of sodium balance.
|
15201541 |
2004 |
|
Hypertensive disease
|
0.300 |
Biomarker
|
group |
RGD |
In ANG II-clamped rats, acute hypertension also provoked disappearance of NHE3 from the apical membranes (27 +/- 2% decrease of total), but NHE3 was shifted to membranes enriched in intermicrovillar cleft and dense apical tubules (step 1) rather than endosomal/lysosomal membranes (step 2).
|
12372791 |
2002 |
|
Hypertensive disease
|
0.300 |
Biomarker
|
group |
RGD |
We conclude that the decrease in renal PT Na(+) transport during acute hypertension is mediated by removal of transport-competent NHE3 from the apical brush border to subapical and internal reserves.
|
11880335 |
2002 |