Cardiac oxidative stress and dysfunction by fine concentrated ambient particles (CAPs) are mediated by angiotensin-II.
Cardiac oxidative stress and dysfunction by fine concentrated ambient particles (CAPs) are mediated by angiotensin-II.
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DOI：
10.3109/08958378.2010.503322
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发表时间：
2010-09
影响因子：
2.1
通讯作者：
Gonzalez-Flecha B
中科院分区：
文献类型：
--
作者：
Ghelfi E;Wellenius GA;Lawrence J;Millet E;Gonzalez-Flecha B
吸入暴露于细微的浓缩环境颗粒（CAP）通过涉及心脏交感神经张力调节的机制增加心脏氧化剂。血管紧张素-II是一种有效的血管收缩剂和参与血压调节的交感神经兴奋肽。我们推测细颗粒暴露后血管紧张素II的增加可能参与心脏氧化应激的发展。在暴露于细PM气溶胶或过滤空气之前，用血管紧张素转换酶（ACE）抑制剂（BenazeTM ®）或血管紧张素受体阻滞剂（ARB，Valsartan ®）处理成年大鼠。在哈佛细颗粒浓缩器（细PM质量浓度：440 ± 80 μg/m3）的室中进行5小时暴露。在暴露结束时，检测动物的心脏原位化学发光（CL）、TBARS和血管紧张素II的血浆水平。此外，还收集了一个暴露动物亚组的连续ECG测量值。PM暴露与血浆血管紧张素浓度的统计学显著增加相关。预处理与ACE抑制剂有效地降低血管紧张素浓度，而ARB治疗导致血管紧张素增加以上的PM-只有水平。PM暴露还导致心脏氧化应激（CL，TBAR）显著增加，ECG上T端至T峰间期缩短，ACE抑制剂和ARB治疗可预防这些情况。这些结果表明，周围的细颗粒物可以增加血浆血管紧张素-II的水平，并建议的作用，在颗粒物相关的急性心脏事件的发展中的肾素-血管紧张素系统。
Inhalation exposure to fine Concentrated Ambient Particles (CAPs) increases cardiac oxidants by mechanisms involving modulation of the sympathovagal tone on the heart. Angiotensin-II is a potent vasoconstrictor and a sympatho-excitatory peptide involved in the regulation of blood pressure. We hypothesized that increases in angiotensin-II after fine PM exposure could be involved in the development of cardiac oxidative stress. Adult rats were treated with an angiotensin converting enzyme (ACE) inhibitor (Benazepril ®), or an angiotensin receptor blocker (ARB, Valsartan ®) before exposure to fine PM aerosols or filtered air. Exposures were carried out for 5 hours in the chamber of the Harvard Fine Particle Concentrator (fine PM mass concentration: 440 ± 80 μg/m3). At the end of the exposure the animals were tested for in situ chemiluminescence (CL) of the heart, TBARS and for plasma levels of angiotensin-II. Also, continuous ECG measurements were collected on a subgroup of exposed animals. PM exposure was associated with statistically significant increases in plasma angiotensin concentrations. Pretreatment with the ACE inhibitor effectively lowered angiotensin concentration, whereas ARB treatment led to increases in angiotensin above the PM-only level. PM exposure also led to significant increases in heart oxidative stress (CL, TBARs), and a shortening of the T-end to T-peak interval on the ECG that were prevented by treatment with both the ACE inhibitor and ARB. These results show that ambient fine particles can increase plasma levels of angiotensin-II and suggest a role of the renin-angiotensin system in the development of particle-related acute cardiac events.
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影响因子：
10.4
作者：
Dockery DW;Luttmann-Gibson H;Rich DQ;Link MS;Mittleman MA;Gold DR;Koutrakis P;Schwartz JD;Verrier RL
通讯作者：
Verrier RL
影响因子：
2.1
作者：
Elder, ACP;Gelein, R;Oberdörster, G
通讯作者：
Oberdörster, G
影响因子：
24.3
作者：
Devlin, RB;Ghio, AJ;Cascio, W
通讯作者：
Cascio, W
DOI：
10.1097/01.asn.0000093235.09769.9c
发表时间：
2004-01-01
影响因子：
13.6
作者：
Berl, T
通讯作者：
Berl, T
影响因子：
3.8
作者：
Ghelfi, Elisa;Ramos-Rhoden, Claudia;Gonzalez-Flecha, Beatriz
通讯作者：
Gonzalez-Flecha, Beatriz