KININS AND ENDOTHELIAL CONTROL OF VASCULAR SMOOTH-MUSCLE

Plasma and vascular kinins stimulate the production of endothelium-der ived nitric oxide, prostacyclin and hyperpolarizing factor (which regu lates the function of vascular smooth muscle), and endothelial interac tions 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 excercise or myoc ardial ischemia indicate that the metabolism of the peptides is fine t uned to the systemic or local metabolic demands. The release of endoth elial vasodilators is impaired (or counterbalanced by the release of c hemical or functional antagonists) in atherosclerosis, hypertension, d iabetes, subarachidonic hemorrhage, and following postischemic injury. ACE-inhibitors potentiate the action of kinins and normalize endothel ial function. in septic shock, hypotension triggered by overproduction of kinins leads to cardiovascular impairment and end-organ damage. Th us the balance in the metabolism of kinins modulates the control of bl ood flow by the endothelium.