Şahintürk Serdar, İşbil Naciye
Department of Physiology, Bursa Uludag University Faculty of Medicine, Bursa, Türkiye.
Turk Gogus Kalp Damar Cerrahisi Derg. 2022 Jan 28;30(1):18-25. doi: 10.5606/tgkdc.dergisi.2022.22756. eCollection 2022 Jan.
This study aims to investigate the roles of potassium channel subtypes in the vasorelaxant effect mechanism of elabela, which is a recently discovered endogenous apelin receptor ligand.
The vascular rings (4-mm) obtained from the thoracic aortas of 20 male Wistar Albino rats were placed into the isolated tissue bath system. The resting tension was set to 1 g. The aortic rings were contracted with 10-5 molar phenylephrine after the equilibration period (90 min). Elabela was applied cumulatively (10-10-10-6 molar) to the aortic rings in the plateau phase. The experimental protocol was repeated in the presence of specific potassium channel subtype inhibitors to determine the role of potassium channels in the vasorelaxant effect mechanism of elabela.
Elabela induced a concentration-dependent vasorelaxation (p<0.001). The maximum relaxation level was approximately 51% according to phenylephrineinduced contraction. Vasorelaxant effect level of elabela statistically significantly decreased after removal of the endothelium (p<0.05). Tetraethylammonium (1 milimolar), 4-Aminopyridine (1 milimolar), glyburide (10 micromolar), and barium chloride (30 micromolar) statistically significantly decreased the vasorelaxant effect level of elabela (p<0.001, p<0.001, p<0.01, and p<0.05 respectively). However, anandamide (10 micromolar) and apamin (100 nanomolar) did not statistically significantly change the vasorelaxant effect level of elabela.
Our results suggest that large-conductance calciumactivated, voltage-gated, adenosine triphosphate-sensitive, and inward-rectifier potassium channels are involved in the vasorelaxant effect mechanism of elabela in the rat thoracic aorta.
本研究旨在探讨钾通道亚型在elabela（一种最近发现的内源性阿片肽受体配体）的血管舒张作用机制中的作用。
从20只雄性Wistar白化大鼠的胸主动脉获取4毫米的血管环，放入离体组织浴系统中。静息张力设定为1克。平衡期（90分钟）后，用10 - 5摩尔的去氧肾上腺素使主动脉环收缩。在平台期将elabela累积应用（10 - 10 - 10 - 6摩尔）于主动脉环。在存在特定钾通道亚型抑制剂的情况下重复实验方案，以确定钾通道在elabela血管舒张作用机制中的作用。
elabela诱导浓度依赖性血管舒张（p<0.001）。根据去氧肾上腺素诱导的收缩，最大舒张水平约为51%。去除内皮后，elabela的血管舒张作用水平在统计学上显著降低（p<0.05）。四乙铵（1毫摩尔）、4 - 氨基吡啶（1毫摩尔）、格列本脲（10微摩尔）和氯化钡（30微摩尔）在统计学上显著降低了elabela的血管舒张作用水平（分别为p<0.001、p<0.001、p<0.01和p<0.05）。然而，花生四烯乙醇胺（10微摩尔）和蜂毒明肽（100纳摩尔）在统计学上并未显著改变elabela的血管舒张作用水平。
我们的结果表明，大电导钙激活、电压门控、三磷酸腺苷敏感和内向整流钾通道参与了elabela在大鼠胸主动脉中的血管舒张作用机制。
