scholarly journals Membrane raft redox signalling contributes to endothelial dysfunction and vascular remodelling of thoracic aorta in angiotensin II‐infused rats

2019 ◽  
Vol 104 (6) ◽  
pp. 946-956 ◽  
Author(s):  
Jian Wei ◽  
Lian Xu ◽  
Ya‐Nan Du ◽  
Xiao‐Feng Tang ◽  
Mao‐Qing Ye ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Thoracic Aorta ◽  
Membrane Raft ◽  
Vascular Remodelling ◽  
Redox Signalling

scholarly journals Membrane raft–lysosome redox signalling platforms in coronary endothelial dysfunction induced by adipokine visfatin

2010 ◽  
Vol 89 (2) ◽  
pp. 401-409 ◽  
Author(s):  
Min Xia ◽  
Chun Zhang ◽  
Krishna M Boini ◽  
Audrey M Thacker ◽  
Pin-Lan Li
Keyword(s):  
Endothelial Dysfunction ◽  
Membrane Raft ◽  
Redox Signalling ◽  
Coronary Endothelial Dysfunction

scholarly journals Toll-like receptor 4 contributes to vascular remodelling and endothelial dysfunction in angiotensin II-induced hypertension

2015 ◽  
Vol 172 (12) ◽  
pp. 3159-3176 ◽  
Author(s):  
R Hernanz ◽  
S Martínez-Revelles ◽  
R Palacios ◽  
A Martín ◽  
V Cachofeiro ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Toll Like Receptor ◽  
Vascular Remodelling ◽  
Toll Like Receptor 4 ◽  
Induced Hypertension

K V 1.3 channels are novel determinants of macrophage‐dependent endothelial dysfunction in angiotensin II‐induced hypertension in mice

2021 ◽  
Vol 178 (8) ◽  
pp. 1836-1854
Author(s):  
Miguel A. Olivencia ◽  
Marta Martínez‐Casales ◽  
Diego A. Peraza ◽  
Ana B. García‐Redondo ◽  
Gema Mondéjar‐Parreño ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Induced Hypertension

Renal endothelial dysfunction and impaired autoregulation after ischemia-reperfusion injury result from excess nitric oxide

2006 ◽  
Vol 291 (3) ◽  
pp. F619-F628 ◽  
Author(s):  
Zhengrong Guan ◽  
Glenda Gobé ◽  
Desley Willgoss ◽  
Zoltán H. Endre
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Tubuloglomerular Feedback ◽  
Sprague Dawley ◽  
Endothelial Nitric Oxide

Endothelial dysfunction in ischemic acute renal failure (IARF) has been attributed to both direct endothelial injury and to altered endothelial nitric oxide synthase (eNOS) activity, with either maximal upregulation of eNOS or inhibition of eNOS by excess nitric oxide (NO) derived from iNOS. We investigated renal endothelial dysfunction in kidneys from Sprague-Dawley rats by assessing autoregulation and endothelium-dependent vasorelaxation 24 h after unilateral (U) or bilateral (B) renal artery occlusion for 30 (U30, B30) or 60 min (U60, B60) and in sham-operated controls. Although renal failure was induced in all degrees of ischemia, neither endothelial dysfunction nor altered facilitation of autoregulation by 75 pM angiotensin II was detected in U30, U60, or B30 kidneys. Baseline and angiotensin II-facilitated autoregulation were impaired, methacholine EC50 was increased, and endothelium-derived hyperpolarizing factor (EDHF) activity was preserved in B60 kidneys. Increasing angiotensin II concentration restored autoregulation and increased renal vascular resistance (RVR) in B60 kidneys; this facilitated autoregulation, and the increase in RVR was abolished by 100 μM furosemide. Autoregulation was enhanced by Nω-nitro-l-arginine methyl ester. Peri-ischemic inhibition of inducible NOS ameliorated renal failure but did not prevent endothelial dysfunction or impaired autoregulation. There was no significant structural injury to the afferent arterioles with ischemia. These results suggest that tubuloglomerular feedback is preserved in IARF but that excess NO and probably EDHF produce endothelial dysfunction and antagonize autoregulation. The threshold for injury-producing, detectable endothelial dysfunction was higher than for the loss of glomerular filtration rate. Arteriolar endothelial dysfunction after prolonged IARF is predominantly functional rather than structural.

The role of TRPV4 channel in the mechanism of angiotensin II-induced endothelial dysfunction

2008 ◽  
Vol 45 (4) ◽  
pp. S27
Author(s):  
Y. Munehisa ◽  
H. Watanabe ◽  
K. Ono# ◽  
H. Ito
Keyword(s):  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Trpv4 Channel

scholarly journals Angiotensin II Impairs Endothelial Nitric-oxide Synthase Bioavailability under Free Cholesterol-enriched Conditions via Intracellular Free Cholesterol-rich Membrane Microdomains

2013 ◽  
Vol 288 (20) ◽  
pp. 14497-14509 ◽  
Author(s):  
Eisuke Amiya ◽  
Masafumi Watanabe ◽  
Norihiko Takeda ◽  
Tetsuya Saito ◽  
Taro Shiga ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Free Cholesterol ◽  
Small Gtpase ◽  
Membrane Microdomains ◽  
No Production ◽  
Aortic Endothelial Cells ◽  
Modified Ldl ◽  
Rich Domain ◽  
Endothelial Nitric Oxide

Vascular endothelial function is impaired in hypercholesterolemia partly because of injury by modified LDL. In addition to modified LDL, free cholesterol (FC) is thought to play an important role in the development of endothelial dysfunction, although the precise mechanisms remain to be elucidated. The aim of this study was to clarify the mechanisms of endothelial dysfunction induced by an FC-rich environment. Loading cultured human aortic endothelial cells with FC induced the formation of vesicular structures composed of FC-rich membranes. Raft proteins such as phospho-caveolin-1 (Tyr-14) and small GTPase Rac were accumulated toward FC-rich membranes around vesicular structures. In the presence of these vesicles, angiotensin II-induced production of reactive oxygen species (ROS) was considerably enhanced. This ROS shifted endothelial NOS (eNOS) toward vesicle membranes and vesicles with a FC-rich domain trafficked toward perinuclear late endosomes/lysosomes, which resulted in the deterioration of eNOS Ser-1177 phosphorylation and NO production. Angiotensin II-induced ROS decreased the bioavailability of eNOS under the FC-enriched condition.

Angiotensin II causes endothelial dysfunction via the GRK2/Akt/eNOS pathway in aortas from a murine type 2 diabetic model

2011 ◽  
Vol 64 (5) ◽  
pp. 535-546 ◽  
Author(s):  
Kumiko Taguchi ◽  
Tsuneo Kobayashi ◽  
Yasuhiro Takenouchi ◽  
Takayuki Matsumoto ◽  
Katsuo Kamata
Keyword(s):  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Diabetic Model ◽  
Type 2 Diabetic

scholarly journals Loss of BReast CAncer Susceptibility Gene 2 Exacerbates Angiotensin‐II‐induced Endothelial Dysfunction

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Alexander Perron ◽  
David Michels ◽  
Hien Nguyen ◽  
Justin Williamson ◽  
Shuhan Bu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Angiotensin Ii ◽  
Endothelial Dysfunction ◽  
Cancer Susceptibility ◽  
Susceptibility Gene ◽  
Breast Cancer Susceptibility ◽  
Breast Cancer Susceptibility Gene ◽  
Cancer Susceptibility Gene
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