Hyperglycemia Does Not Modify the Pupillary Effects of [unk] and k Opiate Agonists in Mice

Abstract

The effects of .mu. and k opiate agonists were assessed on the pupillary size in normoglycemic and hyperglycemic conditions in mice. The .mu. agonists used were, morphine (10, 30 and 100 mg/kg), fentanyl (50, 100 and 150 .mu.g/kg) and sufentanil (5, 10 and 20 .mu.g/kg). The highly selective k opiate agonists used were, U-50488H and U-69593 (30 mg/kg). Chronic hyperglycemia was induced by streptozotocin injection (200 mg/kg i.p.) 7-8 days before the experiment. Acute hyperglycemia was induced by intraperitoneal glucose (5 g/kg i.p) injection at the time of subcutaneous injection of opiates. In the normoglycemic mice, the .mu. agonists produced significant mydriasis (P < 0.05), while k agonists had no effect on the pupil. However, both acute and chronic hyperglycemic condition did not affect the mydriatic ratio of the .mu. opiate agonists. These results indicate that .mu. opiate receptors induce mydriasis in mice and suggest that the hyperglycemia is not the mechanism involved in the opiate induced mydriasis in mice. With the dose of k agonists used, the involvement of k receptors in the pupillary effects in mice were not clear. These results support the hypothesis that hyperglycemia is not the primary mechanism for the altered sensitivity of opiates in the animal models of diabetes.