Hypertension associated with a reduction in renal mass has been traditionally thought of as a volume-dependent state. Recent investigations suggest important roles for systemic and glomerular resistance vessels in the pathogenesis of systemic hypertension (SHT) and progression of end-stage renal disease. To examine this relationship, investigations were performed in two groups of rats maintained for 6 weeks following 5/6 renal ablation. Group A received converting enzyme inhibition (CEI) for 6 weeks. Group B received no treatment. Systolic blood pressure and weight of remnant kidney tissue were both increased in group B (P less than 0.01). BUN did not differ in groups A and B; however, renal PGI2 excretion was increased in group A (P less than 0.01). Renal morphology was preserved in group A, with little or no evidence of glomerular sclerosis. CEI prevents SHT and enhances renal PGI2 excretion in this model. The selective increase in PGI2 may mediate systemic and renal effects of this agent.