Life sciences · 2014
Endothelium-independent vasorelaxation effects of 16-O-acetyldihydroisosteviol on isolated rat thoracic aorta.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Pantan Rungusa, Onsa-Ard Amnart, Tocharus Jiraporn, Wonganan Orawan, Suksamrarn Apichart, Tocharus Chainarong
Аннотация
AIMS: The aim of this study is to investigate the vasorelaxant effect of 16-O-acetyldihydroisosteviol (ADIS) and its underlying mechanisms in isolated rat aorta.
MAIN METHODS: Rat aortic rings were isolated, suspended in organ baths containing Kreb's solution, maintained at 37°C, and mounted on tungsten wire and continuously bubbled with a mixture of 95% O2 and 5% CO2 under a resting tension of 1g. The vasorelaxant effects of ADIS were investigated by means of isometric tension recording experiment.
KEY FINDINGS: ADIS (0.1μM-3mM) induced relaxation of aortic rings pre-contracted by phenylephrine (PE, 10μM) and KCl (80mM) with intact-endothelium (Emax=79.26±3.74 and 79.88±3.79, respectively) or denuded-endothelium (Emax=88.05±3.69 and 78.22±6.86, respectively). In depolarization Ca(2+)-free solution, ADIS inhibits calcium chloride (CaCl2)-induced contraction in endothelium-denuded rings in a concentration-dependent manner. In addition, ADIS attenuates transient contractions in Ca(2+)-free medium containing EGTA (1mM) induced by PE (10μM) and caffeine (20mM). By contrast, relaxation was not affected by tetraethylammonium (TEA, 5mM), 4-aminopyridine (4-AP, 1mM), glibenclamide (10μM), barium chloride (BaCl2, 1mM), and 1H-[1,2,3]oxadiazolo[4,3-α]quinoxalin-1-one (ODQ, 1μM).
SIGNIFICANCE: These findings reveal the vasorelaxant effect of ADIS, through endothelium-independent pathway. It acts as a Ca(2+) channel blocker through both intracellular and extracellular Ca(2+) release.
MAIN METHODS: Rat aortic rings were isolated, suspended in organ baths containing Kreb's solution, maintained at 37°C, and mounted on tungsten wire and continuously bubbled with a mixture of 95% O2 and 5% CO2 under a resting tension of 1g. The vasorelaxant effects of ADIS were investigated by means of isometric tension recording experiment.
KEY FINDINGS: ADIS (0.1μM-3mM) induced relaxation of aortic rings pre-contracted by phenylephrine (PE, 10μM) and KCl (80mM) with intact-endothelium (Emax=79.26±3.74 and 79.88±3.79, respectively) or denuded-endothelium (Emax=88.05±3.69 and 78.22±6.86, respectively). In depolarization Ca(2+)-free solution, ADIS inhibits calcium chloride (CaCl2)-induced contraction in endothelium-denuded rings in a concentration-dependent manner. In addition, ADIS attenuates transient contractions in Ca(2+)-free medium containing EGTA (1mM) induced by PE (10μM) and caffeine (20mM). By contrast, relaxation was not affected by tetraethylammonium (TEA, 5mM), 4-aminopyridine (4-AP, 1mM), glibenclamide (10μM), barium chloride (BaCl2, 1mM), and 1H-[1,2,3]oxadiazolo[4,3-α]quinoxalin-1-one (ODQ, 1μM).
SIGNIFICANCE: These findings reveal the vasorelaxant effect of ADIS, through endothelium-independent pathway. It acts as a Ca(2+) channel blocker through both intracellular and extracellular Ca(2+) release.