Pravastatin Counteracts Angiotensin II-Induced Upregulation and Activation of NADPH Oxidase at Plasma Membrane of Human Endothelial Cells

2010 ◽  
Vol 55 (2) ◽  
pp. 203-212 ◽  
Author(s):  
Ezequiel Alvarez ◽  
Bruno K Rodiño-Janeiro ◽  
Rafael Ucieda-Somoza ◽  
José R González-Juanatey
2008 ◽  
Vol 31 (10) ◽  
pp. 1291-1301 ◽  
Author(s):  
Won Sun Park ◽  
Eun A. Ko ◽  
In Duk Jung ◽  
Youn Kyoung Son ◽  
Hyoung Kyu Kim ◽  
...  

Peptides ◽  
2008 ◽  
Vol 29 (6) ◽  
pp. 1057-1061 ◽  
Author(s):  
Lachlan J. Pearson ◽  
Timothy G. Yandle ◽  
M. Gary Nicholls ◽  
John J. Evans

PLoS ONE ◽  
2013 ◽  
Vol 8 (4) ◽  
pp. e60790 ◽  
Author(s):  
Hitesh M. Peshavariya ◽  
Caroline J. Taylor ◽  
Celeste Goh ◽  
Guei-Sheung Liu ◽  
Fan Jiang ◽  
...  

2010 ◽  
Vol 298 (1) ◽  
pp. F125-F132 ◽  
Author(s):  
Edgar A. Jaimes ◽  
Ping Hua ◽  
Run-Xia Tian ◽  
Leopoldo Raij

Glomerular endothelial cells (GEC) are strategically situated within the capillary loop and adjacent to the glomerular mesangium. GEC serve as targets of metabolic, biochemical, and hemodynamic signals that regulate the glomerular microcirculation. Unequivocally, hyperglycemia, hypertension, and the local renin-angiotensin system partake in the initiation and progression of diabetic nephropathy (DN). Whether free fatty acids (FFA) and reactive oxygen species (ROS) that have been associated with the endothelial dysfunction of diabetic macrovascular disease also contribute to DN is not known. Since endothelial cells from different organs and from different species may display different phenotypes, we employed human GEC to investigate the effect of high glucose (22.5 mmol/l), FFA (800 μmol/l), and angiotensin II (ANG II; 10−7 mol/l) on the genesis of ROS and their effects on endothelial nitric oxide synthase (eNOS), cyclooxygenase-2 (COX-2), and the synthesis of prostaglandins (PGs). We demonstrated that high glucose but not high FFA increased the expression of a dysfunctional eNOS as well as increased ROS from NADPH oxidase (100%) and likely from uncoupled eNOS. ANG II also induced ROS from NADPH oxidase. High glucose and ANG II upregulated (100%) COX-2 via ROS and significantly increased the synthesis of prostacyclin (PGI2) by 300%. In contrast, FFA did not upregulate COX-2 but increased PGI2 (500%). These novel studies are the first in human GEC that characterize the differential role of FFA, hyperglycemia, and ANG II on the genesis of ROS, COX-2, and PGs and their interplay in the early stages of hyperglcyemia.


Hypertension ◽  
2006 ◽  
Vol 48 (5) ◽  
pp. 950-957 ◽  
Author(s):  
Fan Jiang ◽  
Sarah J. Roberts ◽  
Srinivasa raju Datla ◽  
Gregory J. Dusting

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