Recent experimental studies suggest that bradykinin, which induces endothelial release of nitric oxide (NO), prostacyclin, and/or endothelium- derived hyperpolarizing factor, plays an important role in the regulation of vascular tone at rest and during flow-stimulated conditions. In humans, endothelium-dependent vasodilation induced by bradykinin can be blocked by specific B2-receptor blockers, and, in part, by NO synthase. Endogenous bradykinin contributes in an important way to the regulation of coronary vascular tone under resting and flow-stimulated conditions, in human peripheral and coronary arteries. The beneficial effects exerted by the angiotensin-converting enzyme (ACE) inhibitors in heart failure and coronary artery disease could in part be explained by an increased availability of bradykinin, hence improved endothelial function, since ACE is identical to kininase II, which degrades bradykinin...