Increased levels of asymmetric dimethylarginine and C-reactive protein are associated with impaired vascular reactivity in essential hypertension.
Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase and has been implicated in endothelial dysfunction. We sought to assess weather inflammation is involved in the impaired vascular reactivity induced by ADMA in essential hypertension. Brachial artery flow-mediated dilation (FMD), serum ADMA, and C-reactive protein were determined in 71 never-treated hypertensive patients. Serum ADMA was related directly to C-reactive protein and reversely to FMD. In multiple regression analysis, ADMA was the only independent determinant of FMD. Probably, the chronic inflammation documented in these patients may be considered the mechanistic link between ADMA and vascular damage.
Xia
Wei
W
Department of Cardiology, First Affiliated Hospital, Harbin Medical University, Heilongjiang, China.
Feng
Wei
W
Guan
Mingde
M
Yu
Yang
Y
Li
Jingjie
J
Qu
Xiufen
X
D000328:Adult; D000368:Aged; D001120:Arginine / Q000031:analogs & derivatives* / Q000097:blood; D001783:Blood Flow Velocity / Q000502:physiology; D001916:Brachial Artery / Q000503:physiopathology; D002097:C-Reactive Protein / Q000378:metabolism*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology*; D007249:Inflammation / Q000097:blood / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D014664:Vasodilation / Q000502:physiology
C018524:N,N-dimethylarginine; D002097:C-Reactive Protein; D001120:Arginine