Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
In POP<sup>-/-</sup> mice, the increase in Ang-(1-7) was also blunted as compared with WT mice (309±46 and 472±28 fmol/mL, respectively <i>P</i>=0.01), and moreover, the rate of recovery from acute Ang II-induced hypertension was delayed (<i>P</i>=0.016).
|
31786979 |
2020 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Monocyte miR-27a in EVs decreases Mas receptor expression and eNOS phosphorylation in endothelium, impairs Ang-(1-7)-mediated vasodilation and causes hypertension.
|
31328772 |
2020 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
The differential MasR trafficking in neurons from SHRs may contribute to the impaired responses of Ang-(1-7) and to hypertension development.
|
31825460 |
2019 |
Hypertensive disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Hypertension was induced in adult Sprague-Dawley rats by infusion of aldosterone (ALDO; 0.75 μg/hour) for 4 weeks with or without co-treatment of Ang1-7 (1 mg/kg/day).Untreated rats served as controls.
|
30715105 |
2019 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
This study was designed to determine whether inhibition of Ang-(1-7) in the hypothalamic paraventricular nucleus (PVN) attenuates sympathetic activity and elevates blood pressure by modulating pro-inflammatory cytokines (PICs) and oxidative stress in the PVN in salt-induced hypertension.
|
30328008 |
2019 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
These data show that treatment with DIZE or Ang-(1-7) during gestation promoted beneficial effects of attenuating hypertension and cardiac remodeling in adult offspring.
|
31506648 |
2019 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Although further studies are required to determine whether Mito-TEMPO or CAN + Ang-(1-7) treatment at the doses used altered mitochondrial ROS, optimal therapeutic benefits are achieved by shifting the balance from Ang II toward Ang-(1-7) in this model of chronic RAS-dependent hypertension.
|
30540685 |
2019 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
In this study, we have evaluated ACE-inhibitory potential of the tripeptide l-Phenylalanyl-d-Histidyl-l-Leucine (l-Phe-d-His-l-Leu) in vitro and its antihypertensive effect in rat model of dexamethasone-induced hypertension. l-Phe-d-His-l-Leu was custom-designed by changing the configuration of penultimate amino acid residue (histidine) from C-terminal of Ang I, the site at which ACE acts upon and generates Ang II. l-Phe-d-His-l-Leu effectively inhibited ACE activity in a dose-dependent and competitive manner with an IC<sub>50</sub> of 53.32 ± 0.13 nmol/L.
|
30481537 |
2019 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
While the beneficial effects of Ang-(1-7) have been widely studied in several experimental models of hypertension, much less studies were performed in experimental models of atherosclerosis.
|
29541937 |
2018 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
The protective effects of Ang-(1-9) against pulmonary hypertension were inhibited by Ang type 2 receptor (AT<sub>2</sub>R) blocker, but not by Mas receptor blocker.
|
29962859 |
2018 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Large body of experimental data confirmed sustained beneficial effects of ACE2/Ang-(1-7)/Mas receptor axis activation on hypertension and vascular injury.
|
27889958 |
2017 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
The present review examined recent findings regarding the physiological and biological roles of the ACE2‑Ang‑(1‑7)‑Mas axis in the cardiovascular system, discussed potential food‑derived ACE2‑activating agents, and highlighted initiatives, based on this axis, that aim to develop functional foods for the treatment of hypertension.
|
28791402 |
2017 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Ang(1-7) might therefore represent a promising therapy for obstructive sleep apnea-related hypertension and renal injury.
|
28076452 |
2017 |
Hypertensive disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
These alterations indicate an imbalance in the urinary RAAS, promoting the actions of Ang II at the expense of Ang-(1-7), which over time may increase the risk of renal inflammation and fibrosis and ultimately hypertension and renal disease.
|
27636897 |
2017 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Ang 1-7 infusion increased blood pressure, cardiac interstitial fibrosis and cardiac ACE binding compared to untreated STNx rats.
|
28192475 |
2017 |
Hypertensive disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The circulating ACE2 and Ang-(1-7) levels were related to neither rs4646155 nor rs879922 in female or male patients.In conclusion, the rs2106809 polymorphism of the ACE2 gene may be a determinant of the circulating Ang-(1-7) level in female patients with hypertension, suggesting a genetic association between circulating Ang-(1-7) levels and ACE2 gene polymorphisms in patients with hypertension.
|
27310975 |
2016 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Although previous studies have demonstrated that Ang-1 might play an important role in the development of familial pulmonary hypertension, the role of Ang-1 in the development of the pulmonary hypertension associated with CDH is poorly understood.
|
22917924 |
2013 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Differential regulation of signaling pathways in aging and hypertension by Ang II versus Ang-(1-7) may contribute to the autonomic dysfunction accompanying these states.
|
21367658 |
2011 |
Hypertensive disease
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This prevention of hypertension by ACE2 overexpression was reversed by blockade of the Ang-(1-7) receptor (d-Ala7-Ang-[1-7]; 600 ng/kg per minute).
|
19926873 |
2010 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Here we examined whether soluble human recombinant ACE2 (rACE2) can efficiently lower Ang II and increase Ang-(1-7) and whether rACE2 can prevent hypertension caused by Ang II infusion as a result of systemic versus local mechanisms of ACE2 activity amplification. rACE2 was infused via osmotic minipumps for 3 days in conscious mice or acutely in anesthetized mice. rACE2 caused a dose-dependent increase in serum ACE2 activity but had no effect on kidney or cardiac ACE2 activity.
|
19948988 |
2010 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Rodents engineered to express angiopoietin 1 (Ang-1) constitutively in the lung develop severe pulmonary hypertension.
|
14512515 |
2003 |
Hypertensive disease
|
0.100 |
Biomarker
|
group |
BEFREE |
A mechanistic link between familial and acquired pulmonary hypertension was demonstrated by the finding that angiopoietin-1 shuts off the expression of BMPR1A, a transmembrane protein required for BMPR2 signaling, in pulmonary arteriolar endothelial cells.
|
12571257 |
2003 |
Hypertensive disease
|
0.100 |
AlteredExpression
|
group |
BEFREE |
We hypothesized that aberrant expression of the angiopoietin-1 gene in the adult lung would be a major contributing factor in the development of pulmonary hypertension.
|
11436038 |
2001 |