Abstract
Plasma levels of an endogenous nitric oxide (NO) synthase inhibitor, asymmetric dimethylarginine (ADMA), are elevated in a number of disease states including chronic renal failure, pulmonary hypertension, and chronic heart failure. In patients with renal failure, plasma ADMA levels are an independent correlate of left ventricular ejection fraction. However, a causal role for ADMA in the development of cardiovascular disease remains to be demonstrated. In order to test the hypothesis that ADMA has a causal role in disease, we have undertaken molecular and pharmacological approaches to create ex vivo and in vivo systems in which ADMA concentrations are elevated. The role of ADMA in the regulation of vascular function in these model systems will be discussed.
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