This study was conducted as an initial step to elucidate the role of vasopressin in the events leading to irreversible shock. The influence of vasopressin on the maintenance of cardiovascular and respiratory function during early endotoxin shock was evaluated. Conscious, unrestrained male Sprague-Dawley rats (SD) and male homozygous Brattleboro rats (B) lacking vasopressin were anesthetized with 2% enflurane and cannulas were placed in the carotid artery and jugular vein. After recovery from anesthesia, endotoxin (20 mg/kg) was administered. Endotoxin in the B caused an immediate drop in blood pressure to below 40 mm Hg with no recovery. This resulted in death for all ten animals within 3 1/2 hours; eight of ten had expired within 90 min. In contrast, the blood pressure response of the SD dropped to 70 mm Hg but recovered to values near control until sacrificed 240 min after endotoxin. Corticosteroid treatment (300 mg/kg) administered 30 min before endotoxin in the B prevented the severe decrease in blood pressure with values falling to and remaining near 70 mm Hg for the 240-min observation period. All treated animals survived this period. Heart rates in the SD increased sharply after endotoxin and continued to rise, whereas both treated and untreated B increased slowly. Respiration rates for the untreated B were severely depressed until death after endotoxin, whereas the SD and treated B remained at or above control. The results implicate vasopressin in the maintenance of cardiovascular function during the early phase of shock induced by endotoxin, and demonstrate the ability of corticosteroid to substantially improve cardiovascular integrity in the absence of vasopressin.