The Effect of Verapamil on Calcium Transport in the Lens of the Diabetic Rat

Kim, Sang Jin; Kim, Hong Bok

Abstract

Cataracts often occur in diabetic patients or as a consequence of diabetes experimentally induced with alloxan or streptozotocin. In mammals, the transparency of the lens depends on its Ca++ level, and many researchers have proven experimentally that cataracts may occur in cases of increased lens calcium level. In 1981 Fleckenstein et al. were the first to demonstrate experimentally that the cause of cataracts in the alloxan induced diabetic rat is due to an increased lens calcium level, and this calcium induced cataract may be suppressed by the calcium channel blocker-verapamil which prevents lenticular calcium overload. However, they did not determine the mechanism of verapamif on the inhibitory action of lenticular calcium overload. In this experiment verapamil was administrated to control rats and to streptozotocin induced diabetic rats to discover by what mechanism verapamil prevents the occurrence of cataracts as a complication in experimental diabetic rats. The authors compared lens calcium level and measured active 45Ca efflux from the lens, Na+ - Ca++ exchange and Ca++ - ATPase activity in the lens between the control and experimental groups. Their conclusions are as follows: 1. The calcium level of the lens was significantly increased in SDR(Streptozotocin injected diabetic rat) as compared to NDC(Nondiabetic control rat), VNDC(Verapamil treated nondiabetic control rat) and SVDR(Streptozotocin injected verapamil treated diabetic rat). 2. Active 45Ca efflux across the lens membrane was significantly decreased in SDR as compared to NDC, VNDC and SVDR. 3. The Ca++ - ATPase activity was significantly suppressed in SDR as compared to NDC, VNDC and SVDR. 4. Verapamil had no influence on the Na+ - Ca++ exchange transport system in all groups of NDC, VNDC, SDR and SVDR. Thus, our results suggest that verapamil prevents the occurrence of cataracts in diabetic rats probably by controlling the Ca++ transport system in the lens membrane.