Oztürk Y, Aydin S, Ozçelikay A T, Altan V M, Yildizoğlu-Ari N
Department of Pharmacology, Faculty of Pharmacy, Anadolu University, Ankara, Turkey.
Eur J Pharmacol. 1997 Feb 19;321(1):59-65. doi: 10.1016/s0014-2999(96)00928-4.
The effects of experimental diabetes and insulin treatment on the decreased reactivity of isolated rat duodenum to KCl and calmidazolium, a specific calmodulin antagonist, were examined. After 8 weeks of streptozotocin diabetes, the contractile effect of KCl and the non-competitive antagonistic effect of calmidazolium against KCl on isolated rat duodenum were decreased. Calmodulin levels, as measured by radioimmunoassay, were also found to the decreased in duodenum from streptozotocin-diabetic rats. Neither impaired reactivity to KCl nor decreased calmodulin levels in diabetic rat duodenum were corrected by treatment with insulin (10 IU/kg for 20 days). Following insulin treatment, there was only a partial correction in the antagonistic effect of calmidazolium as shown by the increase in non-competitive antagonist affinity constant.
研究了实验性糖尿病及胰岛素治疗对分离的大鼠十二指肠对氯化钾(KCl)反应性降低以及对钙调蛋白特异性拮抗剂氯氮卓酮反应性降低的影响。链脲佐菌素诱导糖尿病8周后,KCl对分离的大鼠十二指肠的收缩作用以及氯氮卓酮对KCl的非竞争性拮抗作用均降低。通过放射免疫测定法测得,链脲佐菌素诱导的糖尿病大鼠十二指肠中的钙调蛋白水平也降低。用胰岛素(10 IU/kg,持续20天)治疗并不能纠正糖尿病大鼠十二指肠对KCl反应性受损以及钙调蛋白水平降低的情况。胰岛素治疗后,氯氮卓酮的拮抗作用仅有部分纠正,表现为非竞争性拮抗剂亲和力常数增加。