The pathogenesis of acute vascular lesions has been studied in two types of accelerated vascular disease. Firstly, vascular lesions were induced by a short-term (2 h) infusion of angiotensin II. Low doses of angiotensin II caused only a slight increase in blood pressure and non-destructive lesions. High doses caused a significant elevation of blood pressure and destructive vascular lesions. Secondly, in renovascular hypertension, renal vascular disease was induced by the removal of the stenosing clip from the renal artery. Incidence and severity of destructive vascular lesions were correlated with the calculated gradient between the pressure before and beyond the stenosis. Anaesthesia had a protective effect on the development of destructive vascular lesions in both models. Obviously, this effect is not related to a reduction of the systemic pressure, but rather to the suppression of abnormal vascular tone, characterized by focal constriction alternating with overdilation. Vasomotor changes, which cause a local overdilation, may be responsible for destructive vascular lesions even at normal to subnormal blood-pressure values. Destructive vascular lesions occur as a result of the exceeding of a critical wall tension. The necrosis of medial smooth-muscle cells in non-destructive lesions may be explained by an excessive contraction, which "surpasses" the metabolic capacity of the cells.