Potassium Channels Contributes to Apelin-induced Vasodilation in Rat Thoracic Aorta

Background: Apelin is a newly discovered peptide hormone and originally discovered endogenous apelin receptor ligand. Objective: In this study, we aimed to investigate the possible roles of potassium channel subtypes in the vasorelaxant effect mechanisms of apelin. Methods: The vascular rings obtained from the thoracic aortas of the male Wistar Albino rats were placed into the isolated tissue bath system. The resting tension was set to 2 g. After the equilibration period, the aortic rings were precontracted with 10-5 M phenylephrine (PHE) or 45 mM KCl. Pyroglutamyl-apelin-13 ([Pyr1]apelin-13), which is the dominant apelin isoform in the human cardiovascular tissues and human plasma, was applied cumulatively (10^-10-10-⁶ M) to the aortic rings in the plateau phase. The experimental protocol was repeated in the presence of specific K⁺ channel subtype blockers to determine the role of K⁺ channels in the vasorelaxant effect mechanisms of apelin. Results: [Pyr1]apelin-13 induced a concentration-dependent vasorelaxation (p < 0.001). The maximum relaxation level was approximately 52%, according to PHE-induced contraction. Tetraethylammonium, iberiotoxin, 4-Aminopyridine, glyburide, anandamide, and BaCl2 statistically significantly decreased the vasorelaxant effect level of [Pyr1]apelin-13 (p < 0.001). However, apamin didn’t statistically significantly change the vasorelaxant effect level of [Pyr1]apelin-13. Conclusion: In conclusion, our findings suggest that BKCa, IKCa, Kv, KATP, Kir, and K2P channels are involved in the vasorelaxant effect mechanisms of apelin in the rat thoracic aorta.