Chronic diabetes and hypertension are associated with increased cataract formation and although the mechanism of cataractogenesis has not been firmly established it has been attributed both to increased polyol pathway and calcium imbalance. In this study we evaluated the effect of decreasing the blood pressure by two different mechanisms on the incidence of cataract formation in streptozotocin diabetic rats. Diabetic rats were treated with either verapamil a calcium channel antoagonist or clonidine a sympathetic nervous system suppressor, for 13 weeks. Blood glucose, insulin, systolic blood pressure, heart rate and frequency of cataract development were monitored during the course of the study. The blood glucoses of the verapamil and clonidine treated animals were not different from untreated diabetics. Untreated diabetics developed significantly higher blood pressures than controls. Verapamil or clonidine treatment inhibited the development of the high blood pressures and maintained them at control levels. The final (13 wks) incidence of cataracts was 75% for the untreated diabetics and the incidence was significantly reduced by verapamil (38%) but not clonidine (63%) treatment. The lenticular calcium content was significantly higher in the diabetics compared to controls. Verapamil treatment decreased the calcium content while clonidine treatment did not. These results suggest that regulation of the calcium imbalance but not hypertension per se can influence cataractogenesis in diabetic animals.