Inhibition of nitric oxide activity by arginine analogs in human renal arteries

Abstract

The results demonstrate that L-NMMA and ADMA reduce basal and stimulated nitric oxide activity in human renal arteries. An increase in the plasma concentrations of methylarginines associated with renal disease should be considered as a risk factor for endothelial dysfunction and abnormal vasomotor tone in human renal arteries.

Plasma concentrations of nitric oxide and asymmetric dimethylarginine in human alcoholic cirrhosis

“…Therefore, it is conceivable that an increase in ADMA in cirrhosis might represent a compensatory mechanism to decrease NO production and, consequently, to counterbalance excessive peripheral vasodilatation. ADMA elicits contractile effects on human renal arteries [24]. Therefore, increased ADMA might be involved in the decrease of renal perfusion and the initiation of functional renal failure in advanced cirrhosis.…”

Asymmetric Dimethylarginine, Blood Pressure, and Renal Perfusion in Elderly Subjects

“…[23][24][25] This has been recently demonstrated by using ADMA in animal experiments and in studies with isolated organs. 26,27 Increased blood levels of ADMA in the elderly may therefore reduce the availability of NO and thus contribute to endothelial dysfunction and arteriosclerosis and finally may lead to increased renovascular resistance and hypertension. 28,29 This hypothesis is supported by the fact that the highest plasma ADMA levels have been found in elderly subjects with the highest FF and/or with the highest RVR, respectively.…”

Elevated plasma adiponectin and decreased plasma homocysteine and asymmetric dimethylarginine in children with type 1 diabetes

“…We measured markers of endothelial activation and inflammation -hsCRP, ICAM-1 and adiponectin -as a marker of anti-atherosclerotic process. As the exact mechanism for increased NO levels in diabetes is not known, we decided to measure ADMA, a powerful endogenous inhibitor of NO production [12], as well. As there are conflicting results regarding whether hyperhomocysteinemia is a cause or a result of CVD [13], we also included tHcy in our panel to clarify its relation with early courses of atherosclerosis.…”