Oner G, Sentürk U K, Izgüt-Uysal V N
Department of Physiology, Faculty of Medicine, Akdeniz University, Antalya, Turkey.
Nephron. 1996;72(2):257-62. doi: 10.1159/000188851.
In order to investigate the role of increased lipid peroxidation in the development of cadmium-induced hypertension, 30 male albino rats were exposed to drinking water containing 15 micrograms/ml cadmium for 30 days, and the results were compared with those of 30 controls. Water containing high cadmium concentrations caused a significant accumulation of the element in blood and kidneys, associated with an obvious elevation in blood pressure. The systolic and diastolic blood pressures rose from 102.8 +/- 7.0 and 81.2 +/- 3.8 mm Hg to 128.1 +/- 4.6 and 107.9 +/- 7.4 mm Hg, respectively, in cadmium-treated rats (p < 0.01). A decreased glomerular filtration rate and increased serum creatinine levels were accompanied by elevated levels of cortical and medullary thiobarbituric acid reactive substances in cadmium-induced hypertensive rats. The mean thiobarbituric acid reactive substance level rose from a control value of 211.5 +/- 64.1 to 303.3 +/- 46.3 nmol/g protein (p < 0.01) in the renal cortex due to the high intake of cadmium. Despite its obvious diuretic and natriuretic action in control animals, the bolus injection of 1.2 and 2.4 micrograms/kg atrial natriuretic peptide corrected neither elevated blood pressure nor the reduced glomerular filtration rate in rats exposed to cadmium. However, the tubular response to atrial natriuretic peptide remained unaltered. These data suggest that a lack of vascular response to atrial natriuretic peptide is one of the many putative causes of cadmium-induced hypertension, and cadmium-mediated increased lipid peroxidation may be involved in this unresponsiveness.
为了研究脂质过氧化增加在镉诱导的高血压发展过程中的作用，将30只雄性白化大鼠暴露于含15微克/毫升镉的饮用水中30天，并将结果与30只对照大鼠的结果进行比较。含高镉浓度的水导致该元素在血液和肾脏中显著蓄积，并伴有血压明显升高。镉处理组大鼠的收缩压和舒张压分别从102.8±7.0和81.2±3.8毫米汞柱升至128.1±4.6和107.9±7.4毫米汞柱（p<0.01）。镉诱导的高血压大鼠肾小球滤过率降低和血清肌酐水平升高，同时皮质和髓质硫代巴比妥酸反应性物质水平升高。由于高镉摄入，肾皮质中硫代巴比妥酸反应性物质的平均水平从对照组的211.5±64.1纳摩尔/克蛋白质升至303.3±46.3纳摩尔/克蛋白质（p<0.01）。尽管心房利钠肽在对照动物中具有明显的利尿和利钠作用，但对暴露于镉的大鼠静脉注射1.2和2.4微克/千克心房利钠肽既不能纠正血压升高，也不能纠正肾小球滤过率降低。然而，肾小管对心房利钠肽的反应保持不变。这些数据表明，对心房利钠肽缺乏血管反应是镉诱导高血压的众多假定原因之一，镉介导的脂质过氧化增加可能与这种无反应性有关。
