KININ RECEPTORS IN THE DIABETIC MOUSE

It has been proposed that kinins are important inflammatory mediators involved in the pathogenesis of several diseases. In the present study , we attempted to determine the effects of kinins in a type I diabetic mouse model, using in vitro assays. Injection of streptozotocin (STZ) to the C57BL/Ks mdb mice causes an insulitis (inflammation of Langerh ans islets) that leads to the diabetic condition. Ten days following t he STZ treatment, the mice showed increased glycemia. We examined the effect of kinins and other agents (substance P, neurokinin A, acetylch oline) on the stomach fundus and urinary bladder of control and diabet ic mice. Our results show that the sensitivity of the stomach findus t o bradykinin (BK) and desArg(9)BK (DBK), but not to other contractile agents, was substantially increased in the tissues of diabetic mice. T he maximal contractions induced by BK and DBK were increased 1.5- to 2 -fold in the stomachs from diabetic mice compared with those from norm al mice. BK induced similar maximal contractions of urinary bladder st rips from normal or STZ-treated mice, while DBK did not show any effec t on this preparation. Interestingly, the apparent affinities of all a gonists are similar in the two groups, normal and diabetic. These resu lts suggest that B-1 and B-2 receptors are overexpressed in the stomac h fundus but not in the urinary bladder of diabetic mice.