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Catcholamine and nitric oxide systems as targets of chronic lead exposure in inducing selective functional impairment

机译：胆碱和一氧化氮系统作为慢性铅暴露的靶标，诱导选择性功能障碍

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Rats were exposed for ten months to 60 ppm of lead (Pb, as acetate) in drinking water to further assess cardiovascular effects of chronic Pb exposure. At the end of the treatment, mean blood Pb was 3.1+/-0.3 mug/dL in the control rats and 22.8+/-1.2 mug/dL in the Pb-exposed rats (means+/-SE, n=12 in each group); these values were not comparable to those of humans. Pb greatly increased plasma levels of noradrenaline (NA) and adrenaline (A), but not those of L-DOPA and dopamine; monoaminoxidase activity was augmented by Pb, mostly in the aorta and in the liver; the aorta, liver, heart and kidney showed discrete histopathological alterations in the Pb-exposed fats, in which plasma levels of nitric oxide (NO, determined as L-citrulline) were reduced. Pb was able to induce blood hypertension, resulting from increase of cardiac inotropism and, mostly, total peripheral resistance. These data were discussed also in relation to those obtained in our previous studies carried out in rats exposed to Pb in drinking water (15-60 ppm) for periods ranging from five to eighteen months. Pb appeared to increase both sympathetic nerve activity by central mechanisms (thus increasing plasma NA and A) and cyclic adenosine monophosphate (cAMP)-dependent availability of calcium ions (Ca++) for contractile mechanisms in the vascular and cardiac myocells (also through an increased vascular alpha (2)- and myocardial beta (1)-adrenoreceptor reactivity). The reduction of plasma NO, contributing to increase vascular resistance and cardiac inotropism, was explained as a result of actions of Pb on enzyme activities concerned with the kallikrein-kinin (KK) and renin-angiotensin-aldosterone (RAA) systems. It was concluded that chronic Pb exposure is able to affect selective neuroendocrine (i,e., catecholamine), autacoidal (i.e., KK and RAA) and transductional pathways (i.e., cAMP, NO, Ca++) involved in the cardiovascular function. (C) 2000 Elsevier Science Inc. All rights reserved. [References: 61]
机译：将大鼠暴露于饮用水中60 ppm的铅（Pb，作为乙酸盐）中暴露10个月，以进一步评估慢性Pb暴露对心血管的影响。在治疗结束时，对照组大鼠的平均血铅为3.1 +/- 0.3马克杯/分升，暴露于铅的大鼠平均血铅为22.8 +/- 1.2马克杯/分升（均值±SE，每组n = 12） ）;这些价值与人类没有可比性。铅会大大增加去甲肾上腺素（NA）和肾上腺素（A）的血浆水平，但不会增加L-DOPA和多巴胺的血浆水平。铅增加了单胺氧化酶的活性，主要在主动脉和肝脏。主动脉，肝脏，心脏和肾脏在暴露于Pb的脂肪中表现出离散的组织病理学改变，其中一氧化氮（NO，确定为L-瓜氨酸）的血浆水平降低。铅能够诱发高血压，这是由于心脏的肌力增加以及大部分外周血总抵抗力增加所致。还讨论了这些数据，这些数据与我们先前在饮用水中（15-60 ppm）暴露于五到十八个月的大鼠中进行的研究中获得的数据有关。铅似乎通过中枢机制增加了交感神经活动（从而增加了血浆NA和A），并依赖循环磷酸一腺苷（cAMP）依赖性钙离子（Ca ++）的利用，从而收缩了血管和心肌细胞的收缩机制（也通过增加了血管） α（2）-和心肌β（1）-肾上腺素受体反应性）。血浆NO减少，有助于增加血管阻力和心脏内向性，被解释为Pb对激肽释放酶激肽（KK）和肾素-血管紧张素-醛固酮（RAA）系统酶活性的作用的结果。结论是，慢性Pb暴露能够影响参与心血管功能的选择性神经内分泌（即儿茶酚胺），autacoidal（即KK和RAA）和转导途径（即cAMP，NO，Ca ++）。 （C）2000 Elsevier Science Inc.保留所有权利。 [参考：61]

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