Plasma and vascular kinins stimulate the production of endothelium-derived nitric oxide, prostacyclin and hyperpolarizing factor (which regulates the function of vascular smooth muscle), and endothelial interactions with blood cells. The role of kinins in vasomotion is determined by the rate of production of the peptides by kininogenases and their degradation by kininases, in particular angiotensin-converting enzyme (ACE). Acute increases in plasma kinin levels during exercise or myocardial ischemia indicate that the metabolism of the peptides is fine tuned to the systemic or local metabolic demands. The release of endothelial vasodilators is impaired (or counterbalanced by the release of chemical or functional antagonists) in atherosclerosis, hypertension, diabetes, subarachidonic hemorrhage, and following postischemic injury. ACE-inhibitors potentiate the action of kinins and normalize endothelial function. In septic shock, hypotension triggered by overproduction of kinins leads to cardiovascular impairment and end-organ damage. Thus the balance in the metabolism of kinins modulates the control of blood flow by the endothelium.