THE EFFECT OF NITRIC OXIDE SYNTHASE ON BETA 3 ADRENOCEPTOR MEDIATED RELAXATION IN STZ DIABETIC RAT HEART

Objective: Beta 3 adrenoceptors have been shown to mediate negative inotropic effect in the heart. In the dibetic rat heart, beta 3 adrenoceptor related relaxation response has been found to be augmented. In the present study, we aimed to investigate the contribution of nitric oxide and nitric oxide synthase subtypes on beta 3 adrenoceptor mediated relaxation response in chronic STZ diabetic rat heart. Material and Method: 8-week old sprague dawley rats were used in the study. Diabetes was induced by single dose streptozotocin injection. Some of the diabetic rats were treated with insulin. Beta 3 adrenoceptor mediated negative inotropic effect was evaluated by using CL 316,243 in the absence and presence of L-NAME. The expression of beta 3 adrenoceptor, eNOS, phosphorylated eNOS and nNOS were determined by western blot experiments. Result and Discussion: The relaxation response was increased in diabetic heart and not normalized after insulin treatment. The effect was abolished after L-NAME incubation. Beta 3 adrenoceptor was upregulated in diabetic heart and reached to control values after treatment. Expression of eNOS, phosphorylated eNOS or nNOS was not altered significantly among the groups. The results of the study indicate that beta 3 adrenoceptor mediated relaxation in diabetic heart is nitric oxide related