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首页> 外文期刊>Biological trace element research >Long-term Mercury Exposure Accelerates the Development of Hypertension in Prehypertensive Spontaneously Hypertensive Rats Inducing Endothelial Dysfunction: the Role of Oxidative Stress and Cyclooxygenase-2
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Long-term Mercury Exposure Accelerates the Development of Hypertension in Prehypertensive Spontaneously Hypertensive Rats Inducing Endothelial Dysfunction: the Role of Oxidative Stress and Cyclooxygenase-2

机译：长期汞曝光加速了诱导内皮功能障碍的预血肿性自发性高血压大鼠高血压的发育：氧化应激和环氧化酶-2的作用

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Mercury is a metal widely dispersed in nature that when in contact with human organism, it damages the cardiovascular system. Long-term mercury exposure for 30 days induces endothelial dysfunction without blood pressure changes in normotensive adult rats. However, it is not known whether exposure to mercury can exacerbate endothelial dysfunction and hypertension development in predisposed animals. Thus, we aimed to investigate the effects of long-term mercury exposure on the blood pressure (BP) and in the isolated aortas of young normotensive and prehypertensive spontaneously hypertensive rats (SHRs). Four-week-old male Wistar rats and SHRs were treated daily with mercury chloride (HgCl2) (1st dose, 4.6 mu g/kg; subsequent dose, 0.07 mu g/kg/day, im, 30 days) or vehicle. BP was assessed weekly and the vascular reactivity to phenylephrine was evaluated in isolated aorta from rats exposed or not to mercury. Mercury exposure did not affect BP in young Wistar rats but accelerated the development of hypertension in young SHRs. Vascular reactivity to phenylephrine increased only in the aorta from mercury-exposed SHRs. While HgCl(2)exposure in SHRs did not alter nitric oxide production, we observed increased superoxide anion production and decreased superoxide dismutase-1 protein expression, and enhanced cyclooxygenase-2 (COX-2) participation with increased prostaglandin (PGE(2)) production and decreased prostacyclin. In the Wistar group, mercury exposure did not alter superoxide anion production or the COX-2 pathway. Mercury exposure accelerated the natural course of hypertension in young SHRs and increased oxidative stress associated with reduced participation of antioxidant enzymes, an activated COX-2 pathway, thereby producing endothelial dysfunction, which is a risk factor in prehypertensive individuals.
机译：汞是一种广泛分散的金属，即在与人体有机体接触时，它会损害心血管系统。长期汞暴露30天诱导内皮功能障碍，没有血压变化的正常成人大鼠。然而，不知道是否暴露于汞可以加剧易患动物的内皮功能障碍和高血压发育。因此，我们旨在探讨长期汞暴露对血压（BP）和年轻正常性和预发性自发性高血压大鼠（SHR）的孤立主动脉的影响。每天用汞氯化物（HgCl2）治疗四周雄性Wistar大鼠和Shrs（第1剂，4.6μg/ kg;后续剂量，0.07μg/ kg /天，Im，30天）或载体。每周评估BP，并在暴露或不汞的大鼠中评价与苯妥妥的血管反应性。汞暴露不影响年轻的Wistar大鼠中的BP，但加速了年轻乳房高血压的发展。对苯肾上肾上腺素的血管反应性仅在汞暴露的SHRS中增加。虽然HGCL（2）在SHR中的暴露没有改变一氧化氮产生，但我们观察到过量的超氧化物阴离子产生和过量的超氧化物歧化酶-1蛋白表达和增强的环氧化酶-2（COX-2）参与前列腺素（PGE（2））生产和减少前列腺素。在Wistar组中，汞暴露未改变超氧化物阴离子生产或COX-2途径。汞暴露加速了年轻乳房高血压的自然过程，增加了与抗氧化酶的参与的增加相关的氧化应激，其活性的COX-2途径，从而产生内皮功能障碍，这是预血压性的危险因素。

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