Acute lead exposure increases arterial pressure: role of the renin-angiotensin system.
Acute lead exposure increases arterial pressure: role of the renin-angiotensin system.
复制标题
DOI：
10.1371/journal.pone.0018730
复制
发表时间：
2011-04-11
期刊：
影响因子：
3.7
通讯作者：
Fioresi M
中科院分区：
文献类型：
--
作者：
Simões MR;Ribeiro Júnior RF;Vescovi MV;de Jesus HC;Padilha AS;Stefanon I;Vassallo DV;Salaices M;Fioresi M
长期接触铅会导致高血压和心血管疾病。我们的目的是评估急性铅暴露对动脉压的影响，并阐明铅诱发高血压发生的早期机制。 Wistar大鼠接受醋酸铅治疗（静脉推注剂量320μg/Kg），并在120分钟内测量收缩动脉压、舒张动脉压和心率。发现动脉压升高，并评估了肾素-血管紧张素系统、Na+,K+-ATP酶和自主神经反射在动脉压升高的这种变化中的潜在作用。在麻醉大鼠中，铅暴露：1) 产生的血铅水平为 37±1.7 µg/dL，低于参考血液浓度 (60 µg/dL)； 2) 动脉收缩压升高（Ct：109±3 mmHg vs Pb：120±4 mmHg）； 3) ACE活性增加（与Ct相比增加27%）和Na+,K+-ATP酶活性（与Ct相比增加125%）； 4) 不改变Na+,K+-ATP酶、AT1和AT2的α1亚基的蛋白质表达。使用 AT1 受体阻滞剂（氯沙坦，10 mg/Kg）或 ACE 抑制剂（依那普利，5 mg/Kg）进行预处理可阻止铅引起的动脉压升高。然而，神经节阻断（六甲铵，20 mg/Kg）并不能阻止铅的高血压作用。急性暴露于低于参考血液浓度的铅会由于 ACE 激活而增加血管紧张素 II 水平，从而增加收缩动脉压。这些发现提供了进一步的证据，表明急性接触铅可以引发高血压发展的早期机制，并且可能是心血管疾病的环境危险因素。
Chronic lead exposure causes hypertension and cardiovascular disease. Our purpose was to evaluate the effects of acute exposure to lead on arterial pressure and elucidate the early mechanisms involved in the development of lead-induced hypertension. Wistar rats were treated with lead acetate (i.v. bolus dose of 320 µg/Kg), and systolic arterial pressure, diastolic arterial pressure and heart rate were measured during 120 min. An increase in arterial pressure was found, and potential roles of the renin-angiotensin system, Na+,K+-ATPase and the autonomic reflexes in this change in the increase of arterial pressure found were evaluated. In anesthetized rats, lead exposure: 1) produced blood lead levels of 37±1.7 µg/dL, which is below the reference blood concentration (60 µg/dL); 2) increased systolic arterial pressure (Ct: 109±3 mmHg vs Pb: 120±4 mmHg); 3) increased ACE activity (27% compared to Ct) and Na+,K+-ATPase activity (125% compared to Ct); and 4) did not change the protein expression of the α1-subunit of Na+,K+-ATPase, AT1 and AT2. Pre-treatment with an AT1 receptor blocker (losartan, 10 mg/Kg) or an ACE inhibitor (enalapril, 5 mg/Kg) blocked the lead-induced increase of arterial pressure. However, a ganglionic blockade (hexamethonium, 20 mg/Kg) did not prevent lead's hypertensive effect. Acute exposure to lead below the reference blood concentration increases systolic arterial pressure by increasing angiotensin II levels due to ACE activation. These findings offer further evidence that acute exposure to lead can trigger early mechanisms of hypertension development and might be an environmental risk factor for cardiovascular disease.
登录
查看更多内容
影响因子：
10.4
作者：
Kosnett MJ;Wedeen RP;Rothenberg SJ;Hipkins KL;Materna BL;Schwartz BS;Hu H;Woolf A
通讯作者：
Woolf A
DOI：
10.1590/s0100-879x2001001000016
发表时间：
2001-10-01
影响因子：
2.3
作者：
Malvezzi, CK;Moreira, EG;Cordellini, S
通讯作者：
Cordellini, S
影响因子：
6.1
作者：
Carmignani, M;Volpe, AR;Felaco, M
通讯作者：
Felaco, M
影响因子：
3.2
作者：
KHALILMANESH, F;GONICK, HC;PURDY, RE
通讯作者：
PURDY, RE
影响因子：
2.8
作者：
Cheng, YW;Schwartz, J;Hu, H
通讯作者：
Hu, H