2006•Zhōnghuá yàoxué zázhìRequires access

Vasodilatation Effects of Rutin in Isolated Thoracic Aorta Rat and Its Underlying Mechanism

Xinmei Zhou, Hui Yao, Yang Jun

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Abstract

OBJECTIVE To determine the possible mechanism in the vasodilatation of rutin on the isolated rat thoracic aorta rings.METHODS Effects of rutin on the contraction of phenylephrine(PE) preconstricted rat thoracic aorta with or without endothelium were determined by organ bath technique.To explore the mechanism,nitric oxide synthase inhibitor L-N(G)-nitroarginine methyl ester(L-NAME),guanylyl cyclase inhibitor methylene blue,cyclooxygenase inhibitor indomethacin,ATP-sensitive K~(+) channel blocker glibenclamide and β-adrenoceptor antagonist propranolol were used.RESULTS Rutin at 10~160 μmol·L~(-1) caused dose-dependent vasorelaxation in endothelium-intact rings preconstricted with PE,but had no effect on aorta rings without endothelium.The maximal response(R_(max)) values calculated from vasorelaxation curves of rutin were(44.28±7.48)%.Pretreatment with L-NAME(0.1 mmol·L~(-1)) or methylene blue(10 μmol·L~(-1)) or indomethacin(10 mmol·L~(-1)) attenuated the vasorelaxation by rutin in endothelium-intact rings.Administration of propranolol(10 μmol·L~(-1)) did not block the vascular effect of rutin.CONCLUSION The results indicate that the vasodilatation of rutin is via nitric oxide-guanylyl cyclase pathway and prostaglandin-mediated mechanism.

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OBJECTIVE To determine the possible mechanism in the vasodilatation of rutin on the isolated rat thoracic aorta rings.METHODS Effects of rutin on the contraction of phenylephrine(PE) preconstricted rat thoracic aorta with or without endothelium were determined by organ bath technique.To explore the mechanism,nitric oxide synthase inhibitor L-N(G)-nitroarginine methyl ester(L-NAME),guanylyl cyclase inhibitor methylene blue,cyclooxygenase inhibitor indomethacin,ATP-sensitive K~(+) channel blocker glibenclamide and β-adrenoceptor antagonist propranolol were used.RESULTS Rutin at 10~160 μmol·L~(-1) caused dose-dependent vasorelaxation in endothelium-intact rings preconstricted with PE,but had no effect on aorta rings without endothelium.The maximal response(R_(max)) values calculated from vasorelaxation curves of rutin were(44.28±7.48)%.Pretreatment with L-NAME(0.1 mmol·L~(-1)) or methylene blue(10 μmol·L~(-1)) or indomethacin(10 mmol·L~(-1)) attenuated the vasorelaxation by rutin in endothelium-intact rings.Administration of propranolol(10 μmol·L~(-1)) did not block the vascular effect of rutin.CONCLUSION The results indicate that the vasodilatation of rutin is via nitric oxide-guanylyl cyclase pathway and prostaglandin-mediated mechanism.

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Available abstract

OBJECTIVE To determine the possible mechanism in the vasodilatation of rutin on the isolated rat thoracic aorta rings.METHODS Effects of rutin on the contraction of phenylephrine(PE) preconstricted rat thoracic aorta with or without endothelium were determined by organ bath technique.To explore the mechanism,nitric oxide synthase inhibitor L-N(G)-nitroarginine methyl ester(L-NAME),guanylyl cyclase inhibitor methylene blue,cyclooxygenase inhibitor indomethacin,ATP-sensitive K~(+) channel blocker glibenclamide and β-adrenoceptor antagonist propranolol were used.RESULTS Rutin at 10~160 μmol·L~(-1) caused dose-dependent vasorelaxation in endothelium-intact rings preconstricted with PE,but had no effect on aorta rings without endothelium.The maximal response(R_(max)) values calculated from vasorelaxation curves of rutin were(44.28±7.48)%.Pretreatment with L-NAME(0.1 mmol·L~(-1)) or methylene blue(10 μmol·L~(-1)) or indomethacin(10 mmol·L~(-1)) attenuated the vasorelaxation by rutin in endothelium-intact rings.Administration of propranolol(10 μmol·L~(-1)) did not block the vascular effect of rutin.CONCLUSION The results indicate that the vasodilatation of rutin is via nitric oxide-guanylyl cyclase pathway and prostaglandin-mediated mechanism.

Key concepts: Phenylephrine, Rutin, Vasodilation, Chemistry, Glibenclamide, Nitric oxide, Pharmacology, Nitric oxide synthase

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