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首页> 外文期刊>African Journal of Biotechnology >Vasorelaxant response induced by Sida santaremnensis H. Monteiro ethanol extract on rat superior mesenteric artery
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Vasorelaxant response induced by Sida santaremnensis H. Monteiro ethanol extract on rat superior mesenteric artery

机译：Sida santaremnensis H.Monteiro乙醇提取物诱导的大鼠肠系膜上动脉的血管舒张反应

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摘要

The aim of this work was to characterize the vasorelaxant effect produced by?Sida santaremnensis?ethanol extract (Ssan-EtOH) in rat superior mesenteric artery. Ssan-EtOH showed neither acute toxicity nor hemolytic activity. In the other hand, it induced a concentration-dependent vasorelaxant effect on phenylephrine (10 μmol/L) or KCl (80 mmol/L)-induced pre-contractions in endothelium-intact rat mesenteric artery rings, which attenuated after endothelium removal, without changes in maximum effect.?NG-nitro-L-arginine methyl ester?(L-NAME) (100 μmol/L), indomethacin (10 μmol/L), atropine (1 nmol/L), KCl (20 mmol/L) or tetraethylammonium (3 mmol/L) pretreatment also induced a response attenuation. The endothelium-derived hyperpolarizing factor (EDHF) involvement in Ssan-EtOH-induced vasorelaxant response was verified after L-NAME (100 μmol/L) plus Indomethacin (10 μmol/L) plus tetraethylammonium (3 mmol/L) pretreatment and this vasorelaxation was decreased. In endothelium-denuded rings, Ssan-EtOH was able to inhibit phenylephrine-induced contractions (10-9?to 10-5?mol/L) in a concentration-dependent manner. In a nominally without Ca2+?depolarizing Tyrode solution, Ssan-EtOH inhibited CaCl2?(10-6?– 3 x 10-2?mol/L)-induced contractions in a concentration-dependent manner. The endothelium-dependent Ssan-EtOH-induced vasorelaxant effect probably involves the participation of the?nitric oxide synthase (NOS) and cyclooxygenases (COX)?pathways, as well muscarinic receptors and EDHF and the endothelium-independent effect probably occurs by Ca2+?influx inhibition through voltage-operated calcium channels.
机译：这项工作的目的是表征？Sida santaremnensis？乙醇提取物（Ssan-EtOH）对大鼠肠系膜上动脉产生的血管舒张作用。 Ssan-EtOH既没有显示出急性毒性也没有溶血活性。另一方面，它对完好无损的大鼠肠系膜动脉环中苯肾上腺素（10μmol/ L）或KCl（80 mmol / L）诱导的预收缩诱导了浓度依赖性血管舒张作用，该作用在去除内皮后减弱。 NG-硝基-L-精氨酸甲酯？（L-NAME）（100μmol/ L），消炎痛（10μmol/ L），阿托品（1 nmol / L），KCl（20 mmol / L） ）或四乙铵（3 mmol / L）预处理也会引起反应减弱。在L-NAME（100μmol/ L）加消炎痛（10μmol/ L）加四乙铵（3 mmol / L）预处理和此血管舒张后，证实了内皮源超极化因子（EDHF）参与Ssan-EtOH诱导的血管舒张反应。减少了。在内皮剥脱的环中，Ssan-EtOH能够以浓度依赖的方式抑制去氧肾上腺素引起的收缩（10-9？至10-5？mol / L）。在名义上没有Ca2 +β去极化的Tyrode溶液中，Ssan-EtOH以浓度依赖的方式抑制CaCl2β（10-6β-3x10-2μmol/ L）诱导的收缩。内皮依赖性的Ssan-EtOH诱导的血管舒张作用可能涉及一氧化氮合酶（NOS）和环氧合酶（COX）途径，以及毒蕈碱受体和EDHF的参与，内皮依赖性作用可能是由Ca2 +涌入引起的。通过电压操纵的钙通道抑制。

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