FIGURE 1 Blood flow in the coronary vessel causes deformation of the endothelial cell. In response to shear stress, endothelial NO synthase elaborates NO from L-arginin, which diffuses rapidly into smooth muscles in the vessel wall and results in sequestration of intracellular Ca++ and consecutive vasodilation.
Smooth muscle cell
NADPH-oxidase and xanthin-oxidase, are responsible for NO-degradation in the first line (24, 25). In addition ROS oxidate tetrahydrobiopterin, an essential cofactor of eNOS. This leads to an uncoupling of eNOS, which now starts to produce oxygen radicals instead of NO, further aggravating endothelial dysfunction (17, 26).
To counterbalance premature NO degradation a number of enzymatic and nonenzymatic protective mechanisms are available within the endothelium; the most important are superoxide dismutase (SOD), extracellular SOD, glutathionperoxidase, catalase, and thior-edoxin/thioredoxin-reductase.
A previously published study showed that endothelial dysfunction may be corrected by regular physical exercise in patients with congestive heart failure or atherosclerotic heart disease (Fig. 2) (27). Patients with stable angina pectoris were randomized between an active intervention group, which exercised on stationary bicycles, and an inactive control group. At baseline endothelial function was assessed by intracoronary infusion of acetylcholine, which was highly abnormal in both groups. Following 4 weeks of submaximal exercise paradox vasoconstriction in response to acetylcholine was reduced by 54%. Peak blood flow velocity in response to intracoronary adenosine, representing coronary vasodilatory reserve, improved by 64%. This finding may in part explain the reduction of anginal symptoms frequently observed in patients exercising on a regular basis.
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