Vasorelaxation effect of 18β-glycyrrhetinic acid on the thoracic aorta of rats: proposed mechanism
18β-Glycyrrhetinic acid (18β-GA) is an effective component extracted from the traditional Chinese medicine Radix glycyrrhizae (Leguminosae) and has various biological activities. This study was performed to investigate the vasodilatory effects of 18β-GA on isolated rat thoracic aortic rings and explore the underlying mechanisms. The rings were obtained from normal Sprague–Dawley rats and then precontracted with norepinephrine (NE) (1 μM) or KCl (60 mM). 18β-GA (1.883–11.297mg/L) was added successively by cumulative dosing to observe and record the changes in the tension of the vascular ring. The effects of NG-nitro-l-arginine methylester (L-NAME), indomethacin (INDO), barium chloride (BaCl2), 4-aminopyridine(4-AP), tetraethylammonium (TEA), and glibenclamide on the vascular diastolic function of 18β-GA were determined. 18β-GA substantially exhibited a dose-dependent vasorelaxant effect on the NE-induced and KCl-induced contractions of the rings. The integrity of the vascular endothelium had no influence on the 18β-GA-induced vasorelaxation effect in the rings. L-NAME and IDON showed no significant differences in their effects on this vasorelaxation process in the rings precontracted with NE. This result suggests that the vasorelaxation mechanism of 18β-GA may be independent of the vascular endothelium . BaCl2 and 4-AP antagonized the vasorelaxation effect of 18β-GA, but TEA and glibenclamide showed no remarkable effect on the vasodilation of 18β-GA. Findings suggest that 18β-GA induces vasorelaxation in thoracic aortic rings via the receptor-operated Ca2+ channels and voltage-operated Ca2+ channels and the opening of inward rectifier potassium channels and voltage-operated potassium.
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Document Type: Research Article
Publication date: December 1, 2019
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