The effect of tempol administration on the aortic contractile responses in rat preeclampsia model.

ISRN Pharmacology Pub Date : 2012-01-01 Epub Date: 2012-09-03 DOI:10.5402/2012/187208
Mohammad Sharif Talebianpoor, Hossein Mirkhani
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引用次数: 22

Abstract

It is reported that reactive oxygen species production has a critical role in the manifestations and complications of preeclampsia. In the present study, the effect of tempol on the response changes of aortic rings of preeclamptic rats has been studied. Preeclamptic rats (induced by L-NAME) were treated with three different oral doses of tempol (20, 60 and 180 mg/kg/day) from the Day 10 of gestation. Systolic blood pressure, plasma malondialdehyde and 8-isoprostane and the vascular effects of phenylephrine, calcium, acetylcholine and diazoxide were the studied parameters. L-NAME administration resulted in hypertension, proteinuria, increased oxidative stress markers, increased vascular sensitivity to phenylephrine and decreased sensitivity to acetylcholine in pregnant rats. No significant changes in response to calcium and diazoxide were observed. Tempol at doses of 20 and 60 mg/kg/day significantly reversed these changes but at a high dose (180 mg/kg/day), it had no significant effect and in some cases intensified the effect. These results revealed that in the experimental preeclampsia, the sensitivity of rat aorta to alpha- adrenergic receptor agonists was increased and its endothelium-dependent relaxation was decreased. Tempol at lower used doses reduced the blood pressure and oxidative stress and restored the normal responsiveness of vascular tissue in preeclamptic rats.

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大鼠子痫前期模型大鼠主动脉收缩反应的影响。
据报道,活性氧的产生在子痫前期的表现和并发症中起着关键作用。本研究研究了天麻酚对子痫前期大鼠主动脉环反应变化的影响。子痫前期大鼠(L-NAME诱导)从妊娠第10天开始口服三种不同剂量的天酚(20、60和180 mg/kg/天)。研究收缩压、血浆丙二醛和8-异前列腺素以及苯肾上腺素、钙、乙酰胆碱和二氮氧化合物对血管的影响。L-NAME可导致妊娠大鼠高血压、蛋白尿、氧化应激标志物升高、血管对苯肾上腺素敏感性升高、对乙酰胆碱敏感性降低。对钙和二氮氧化合物的反应无明显变化。20和60 mg/kg/天剂量的天冬酚显著逆转了这些变化,但在高剂量(180 mg/kg/天)时,它没有显著作用,在某些情况下还会增强这种作用。结果表明,实验性子痫前期大鼠主动脉对α -肾上腺素能受体激动剂的敏感性增加,内皮依赖性松弛降低。低剂量的天酚降低了子痫前期大鼠的血压和氧化应激,恢复了血管组织的正常反应性。
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