Liquiritin Promotes Vasodilation Effects by Activating the K _v and K _ATP Channels in the Isolated Rat Thoracic Aorta

Background Liquiritin, a flavonoid present in the traditional Chinese medicine Radix Glycyrrhizae , reduces myocardial damage and improves cardiac function. However, it remains unclear what effect it has on the thoracic aortic rings. Objectives Use of rat thoracic aortic rings to study the vasodilatory effects of liquiritin and its associated mechanisms. Materials and Methods The arterial tension of rat thoracic aortic rings was measured in vitro using the perfusion method. Precontraction of the thoracic aortic rings with phenylephrine (PE) 1 µM and changes in vascular ring tension were observed and recorded after cumulative administration of liquiritin (1, 3, 10, 30, 100, and 300 µM). The effects of liquiritin on the tension of thoracic aortic rings with intact or denuded endothelial that were precontracted with PE or potassium chloride were determined, as well as how NG-nitro- l -arginine methyl ester (L-NAME), 4-aminopyridine (4-AP), indomethacin (INDO), tetraethylammonium (TEA), barium chloride (BaCl 2 ), and glibenclamide (Gli) affected the vasodilatory function of liquiritin. Results Liquiritin exerts a diastolic effect on PE-induced contraction of the thoracic aortic ring, and this effect is independent of the integrity of the vascular endothelium. L-NAME and INDO pretreatment also did not influence the vasodilatory function of liquiritin, illustrating that it might not be endothelium-dependent. Furthermore, pretreatment with TEA, a Ca 2+ -activated K + channel inhibitor, and BaCl 2 , an inwardly rectifying K + channel inhibitor, did not affect the vasodilatory effects of liquiritin. Nevertheless, pretreatment with the voltage-dependent K + (K v ) channel inhibitor, 4-AP, and the ATP-sensitive K + (K ATP ) channel inhibitor, Gli, significantly reduced the vasodilatory effect of liquiritin, indicating that the vasodilatory effects of liquiritin may have a bearing on the activation of K v and K ATP channels. Conclusion Overall, we confirmed for the first time that liquiritin has vasodilatory effects that are endothelium-independent, and the mechanism of its vasodilatory effect may include activation of K v and K ATP channels.