Acute pressor responses to angiotensin, renal extract, and noradrenaline caused irregularity of calibre in the mesenteric arterioles of the rat. The dilated segments of arterioles were permeable to intravenously injected carbon particles, the constricted segments were not. The degree of carbon deposition was related to the mean arterial pressure and not to the dose or nature of the pressor substance. It is suggested that carbon deposition is the result of structural damage to the vessel wall caused by the inability of vascular smooth muscle to withstand high arterial pressure. No evidence was found for the action of a vascular permeability factor of renal origin.