The effect of acute hemorrhage on hemodynamics and the renin-angiotensin system (RAS) was studied in eight anesthetized dogs. Stepwise blood loss to 17 +/- 6.2 ml/kg within 9 to 33 min decreased cardiac output (CO) to 42.8% of control. Mean arterial blood pressure was decreased to 35%, peripheral vascular resistance (PVR) was 1.58-fold increased, plasma renin activity (PRA) and plasma renin concentration (PRC) were increased 3.6-fold and 4.3-fold, respectively, angiotensin I (A I) concentration in plasma was 3.7-fold increased, angiotensin II (A II) was 3.8-fold increased, and A I-degrading enzyme was strongly decreased. Angiotensinogen, A I-converting enzyme, and A II-degrading enzyme activities into blood circulation were not significantly changed. The minimal blood loss to activate the RAS was 3 ml/kg. The rate of plasma active renin (PRA and PRC) increase depended on the velocity of blood withdrawn. PRA was correlated inversely to CO. PVR correlated linearly to increased plasma angiotensin concentrations. The experiments conducted demonstrate the high sensitivity and prompt activation of RAS to blood loss and suggest that RAS is involved in the regulating mechanisms of hemodynamics during acute graded hemorrhage. The stimulation of RAS supports survival of grave blood loss.