enalapril and Cataract

Previously, we assessed that hypertension increases cataractogenesis. In the present study, we evaluated the effect of oral and topical administration of enalapril on two kidney one clip (2K1C)-induced hypertensive cataract model by evaluating the biochemical alteration of lenticular antioxidants, ionic content, ATPase activity, protein content and careful examination of the lenticular opacity.. Animals were divided into normal and hypertensive animals. Hypertensive animals were divided into hypertensive control group (0.3% CMC), enalapril (oral) treatment group (20 mg/kg/day; p.o), and enalapril (topical) treatment group (0.1% w/v on the eye cornea) for a period of twelve weeks. During experimental study blood pressure, heart rate and morphology of the eyes were monitored biweekly. After twelve weeks, lenses were photographed and various catractogenic biochemical parameters were assessed.. Enalapril (oral) treatment conserved the blood pressure (systolic and diastolic), restored the level of antioxidants, restored the lipid peroxidation marker, nitrite content, ionic content, ATPase function, protein content, and thus delayed the cataract formation. While, enalapril (topical) treatment exhibited anti-cataract effect without affecting the systolic and diastolic blood pressure that could be by restoring the antioxidant level, maintaining the ionic balance, balancing the protein levels, and by inhibiting the upregulated ocular renin angiotensin system. The overall results suggest that enalapril (topical) treatment showed conspicuous effect than enalapril (oral) treatment in adjourning the cataract formation.. Based on the results, it may be concluded that upregulated ocular RAS by increasing oxidative stress and by misbalancing the lenticular ionic and protein content may lead to cataract formation in hypertensive condition.

Topics: Adenosine Triphosphatases; Administration, Topical; Angiotensin-Converting Enzyme Inhibitors; Animals; Antioxidants; Blood Pressure; Cataract; Enalapril; Hypertension; Kidney; Rats; Rats, Sprague-Dawley; Surgical Instruments

Hyperglycemia enhances cataractogenesis. Elevated glucose level is commonly accompanied by arterial hypertension, for which angiotensin-converting enzyme (ACE) inhibitors (ACEIs) are a widely used intervention. ACE inhibitors exert some endothelial pleiotropic actions and can beneficially modulate glucose control and some other metabolic pathways. The purpose of this study was to evaluate the effect of ACEIs on cataract formation in experimental alloxan-induced diabetes in rabbits and assess the role of the reactive function group of the ACEIs in this process.. Two study and two control groups of rabbits were examined. In the study groups and in one of the control groups, diabetes was induced by alloxan. The study groups were assigned to receive captopril or enalapril for six months; the controls received distilled water. Glucose concentration was monitored with a glucometer. A biomicroscope and an ophthalmoscope were used to evaluate lens opacity and cataractogenesis.. Six-month administration of ACEI to rabbis resulted in a delay of diabetic cataractogenesis. The rate of cataract formation was significantly lower in the group treated with captopril than in the enalapril group. A difference in morphology of lens opacity formation between the two study groups was observed.. ACEIs delay diabetic cataractogenesis in an experimental animal model. The ACEI functional groups have different influences on the pattern and rate of lens opacity.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Glucose; Captopril; Cataract; Diabetes Mellitus, Experimental; Enalapril; Rabbits