The purpose of this study was to determine whether the renin-angiotensin system (RAS), nitric oxide (NO), atrial natriuretic peptide (ANP), blood pressure (BP), ultrastructural characteristics, and endothelium-dependent relaxation of thoracic aorta were modulated by the estrogen level. Rats were divided into 3 groups: ovariectomized (OVX); not ovariectomized (sham); and ovariectomized and treated with subcutaneous 17beta-estradiol (15 microg/kg/day, OVX+E(2)) (n=15-17 per group). For 13 weeks after surgery, blood pressure, serum estrogen, NO, plasma angiotensin II (Ang II), ANP, and renin activity levels were monitored. Thirteen weeks after surgery, the vasodilator responses of the aortic rings to acetylcholine and the ultrastructural characteristics of the thoracic aorta were determined. In the 9th and 13th week, OVX rats had a significantly higher blood pressure than the other two groups (p<0.05). Ovariectomy led to a significant decrease in plasma Ang II level and a significant increase in renin activity in OVX rats compared to sham rats; this effect could be reversed by estrogen treatment. In the 5th, 9th, and 13th weeks, the serum NO level was significantly lower in the OVX group than in the sham group (p<0.05); this effect could be reversed by estrogen treatment. Plasma ANP levels in the 9th and 13th weeks were significantly lower in the OVX group (p<0.05), and plasma ANP levels could be completely restored by estrogen treatment. Ovariectomy markedly reduced endothelium-dependent relaxation in response to acetylcholine in isolated rat thoracic aortic rings; chronic estrogen treatment significantly restored endothelium-dependent relaxation in response to acetylcholine. Under electron microscopy, the endothelial cells in OVX rats were swollen, even necrosed; estrogen treatment inhibited these changes. These results strongly suggest that estradiol protects rats from the development of hypertension and has a protective effect on the endothelium by increasing NO and ANP levels while decreasing renin activity. However, there was a discordance between the effects that estradiol had on angiotensin II and on blood pressure. This might be the result of negative feedback that ultimately results in the overall suppression of the RAS.

译文

:本研究的目的是确定是否存在肾素-血管紧张素系统(RAS),一氧化氮(NO),心房利钠肽(ANP),血压(BP),超微结构特征和胸主动脉内皮依赖性舒张由雌激素水平调节。将大鼠分为3组:去卵巢的(OVX);去卵巢的(OVX)。未切除卵巢(假);并经皮下注射17β-雌二醇(15微克/千克/天,OVX E(2))进行去卵巢和处理(每组n = 15-17)。术后13周,监测血压,血清雌激素,NO,血浆血管紧张素II(Ang II),ANP和肾素活性水平。术后十三周,确定主动脉环对乙酰胆碱的血管舒张反应和胸主动脉的超微结构特征。在第9周和第13周,OVX大鼠的血压明显高于其他两组(p <0.05)。与假手术大鼠相比,卵巢切除术可导致OVX大鼠血浆Ang II水平显着降低,肾素活性显着提高。这种作用可以通过雌激素治疗来逆转。在第5、9和13周,OVX组的血清NO水平显着低于假手术组(p <0.05)。这种作用可以通过雌激素治疗来逆转。 OVX组第9周和第13周的血浆ANP水平显着降低(p <0.05),并且通过雌激素治疗可以完全恢复血浆ANP水平。卵巢切除术显着降低了离体大鼠胸主动脉环对乙酰胆碱的内皮依赖性舒张反应;慢性雌激素治疗可显着恢复对乙酰胆碱的内皮依赖性舒张反应。在电子显微镜下,OVX大鼠的内皮细胞肿胀甚至坏死。雌激素治疗抑制了这些变化。这些结果强烈表明,雌二醇可保护大鼠免于高血压的发展,并通过增加NO和ANP的水平同时降低肾素的活性而对内皮具有保护作用。但是,雌二醇对血管紧张素II和血压的影响之间存在分歧。这可能是负反馈的结果,最终导致对RAS的整体抑制。

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