The role of nitric oxide in heart failure is unknown. The high-capacit
y inducible isoform of nitric oxide synthase is present in the myocard
ium of patients with idiopathic dilated cardiomyopathy. Plasma nitrate
, the stable end-product of nitric oxide production, was significantly
increased in patients with heart failure compared with normal control
s (means 51.3 and 24.6 mu mol/L). Vasodilation caused by increased nit
ric oxide may compensate for the vasoconstrictor effect of neurohumora
l adaptions to heart failure. Alternatively, excess production may be
detrimental to the heart by a direct negative inotropic effect.