The vascular endothelium is a source of substances particularly nitric oxid
e that act in a paracrine fashion either to contract or relax smooth muscle
cells and this function is disturbed in atherosclerotic arteries. The endo
thelium derived nitric oxide contribute in the basal vasomotor tone of epic
ardial normal and atheromatous coronary coronary arteries, and of atheromat
ous coronary stenoses in patients with stable angina. Nitrates, by acting i
ndirectly to increase cGMP in smooth muscle cells, dilate most coronary ste
noses and normal coronary segments, decrease left ventricular afterload and
diastolic filling pressure and improve the distribution of coronary flow t
o subendocardial zone. Large and small epicardial coronary vessels responde
d differently to endothelium-dependent and independent vasodilators.