Selective renal medullary destruction is produced in rats by a single injection of 2- bromoethylamine hydrobromide. The object of these studies was to investigate whether destruction of the renal medulla in normal rats would alter vascular capacitance. Conscious bromoethylamine-treated rats (n= 15) were compared with control saline-injected rats (n= 12). Mean circulatory filling pressure was measured during a brief circulatory arrest caused by inflation of a right atrial balloon. Blood volume was determined from plasma volume (iodine-125-labeled albumin) and hematocrit. Mean circulatory filling pressure was measured at resting blood volume and after rapid blood volume changes. Vascular compliance was derived from the mean circulatory filling pressure-blood volume curve. The bromoethylaminetreated rats were significantly hypertensive compared with control rats (mean arterial pressure 133±2 and 114±3 mm Hg, respectively,p< 0.001) and had a significant tachycardia (475±8 and 443 ±10 beats/min, respectively, p=0.02). Blood volume, plasma volume, hematocrit, and sodium excretion were no different There was no significant difference in mean circulatory filling pressure (6.5±0.2 and 6.8±0.2 mm Hg, respectively, p=0.4) or vascular compliance (3.64±0.20 and 3.53±0.12 ml/kg/mm Hg, respectively, p=0.7). The position of the vascular pressure-volume curve was unchanged indicating no change in vascular capacity. This would suggest that the destruction of renal medullary vasodepressor mechanisms does not result in alterations in vascular capacitance.