Khoshavi Najafabadi Fatameh, Sadraei Hassan, Mehranfard Nasrin, Ghasemi Maedeh
Department of Pharmacology and Toxicology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran.
Neurophysiology Research Center, Cellular and Molecular Medicine Research Institute, Urmia University of Medical Sciences, Urmia, Iran.
Adv Biomed Res. 2023 Jul 27;12:199. doi: 10.4103/abr.abr_44_23. eCollection 2023.
The goal of the current research was to further elucidate the role of adenosine triphosphate (ATP)-sensitive potassium (K) channels in the motility and contractility force of gastric smooth muscle of diabetic rats.
Male Wistar rats (190-230 g) were grouped into control and streptozotocin (STZ)-induced diabetes (55 mg/kg) rats. Thirty days later, gastric muscle contractility was measured using a myograph and a force transducer of antral segments immersed in a tissue bath. Gastric emptying response was measured through feeding of standard pellet. Furthermore, the expression of K channel subunits in antral smooth muscle was determined by western blot technique.
The amplitude of KCl-evoked twitch contractions of diabetic antral strips was about 25% more than control ( < 0.05). Application of minoxidil, a K channel opener, dose dependently decreased the force of twitch contractions in both normal and diabetic antral strips. Application of 10 μM glibenclamide, a K channel blocker, did not antagonize the minoxidil-induced relaxation of antral strips. Diabetic gastric emptying was faster than normal, although not significant. Despite the relaxant effect of minoxidil on gastric emptying rate in normal rats ( < 0.05), this effect was not observed in diabetic rats. Also, glibenclamide increased gastric emptying and antagonized minoxidil-induced relaxation in normal rats ( < 0.05). Furthermore, the expression of K Kir6.1 and SUR2B subunits was substantially reduced in antral smooth muscle in diabetic condition ( < 0.01).
These results propose that K channels may contribute to the development of gastric motility disorders in diabetes.
当前研究的目的是进一步阐明三磷酸腺苷（ATP）敏感性钾（K）通道在糖尿病大鼠胃平滑肌运动性和收缩力中的作用。
将雄性Wistar大鼠（190 - 230克）分为对照组和链脲佐菌素（STZ）诱导的糖尿病组（55毫克/千克）。30天后，使用肌动描记器和置于组织浴中的胃窦段力传感器测量胃肌收缩力。通过喂食标准颗粒测量胃排空反应。此外，采用蛋白质免疫印迹技术测定胃窦平滑肌中钾通道亚基的表达。
糖尿病胃窦条带中氯化钾诱发的抽搐收缩幅度比对照组高约25%（P < 0.05）。钾通道开放剂米诺地尔的应用，剂量依赖性地降低了正常和糖尿病胃窦条带的抽搐收缩力。钾通道阻滞剂10 μM格列本脲的应用并未拮抗米诺地尔诱导的胃窦条带松弛。糖尿病大鼠的胃排空比正常大鼠快，尽管差异不显著。尽管米诺地尔对正常大鼠胃排空率有松弛作用（P < 0.05），但在糖尿病大鼠中未观察到这种作用。此外，格列本脲增加了正常大鼠的胃排空并拮抗了米诺地尔诱导的松弛（P < 0.05）。此外，在糖尿病状态下，胃窦平滑肌中K Kir6.1和SUR2B亚基的表达显著降低（P < 0.01）。
这些结果表明钾通道可能在糖尿病胃动力障碍的发生中起作用。
