In never-treated hypertensive patients, elevated ADMA levels are independently associated with impaired flow-mediated dilation and correlate with CRP, suggesting a link between inflammation, ADMA, and endothelial dysfunction.
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 et al. (Mon,) studied this question.