Blood pressure elevation by heavy metals, its mechanism and prevention

1)正常大鼠和自发性高血压（SHR）大鼠分别给予含CdCl_2颗粒食物15 g/d，剂量分别为0、3、30和300ppm。年龄相关的收缩压升高仅在暴露于3ppm Cd的SHR大鼠中加速，而暴露于300ppm Cd的SHR大鼠则被抑制。这可能表明，只有在具有高血压遗传的受试者中，较低剂量的Cd才会加速收缩压。收缩压降低可能是Cd中毒的征兆。2)正常大鼠和自发性高血压大鼠分别给予15 g/d含PbCl_2的颗粒食物，剂量分别为0、3、30和300 ppm。年龄相关性的收缩压升高仅在暴露于3ppm Pb的SHR大鼠中加速。这可能表明，只有在有高血压遗传的受试者中，低剂量的铅才会加速收缩压。补充研究表明，较低剂量（0.3 ppm和1 ppm）的铅更明显地加速了年龄相关的收缩压升高，并且动脉粥样硬化可能通过异常胆固醇代谢加速血压升高。3)正常大鼠和自发性高血压大鼠分别给予含HgCl_2颗粒食物15 g/d，剂量分别为0、1、3、10和30 ppm。年龄相关性收缩压升高仅在暴露于所有水平汞的SHR大鼠中加速。生化数据表明，动脉粥样硬化可能通过汞引起的胆固醇代谢异常而加速年龄相关性收缩压升高。

1) Both normotensive and spontaneously hypertensive (SHR) rats were given 15 g/day pelleted food containing CdCl_2 at a dose level of 0,3,30 or 300 ppm. Age-related elevation in systolic blood pressure was accelerated only in SHR rats exposed to 3 ppm Cd, but was depressed in SHR rats exposed to 300 ppm Cd. This might suggest that systolic blood pressure is accelerated by Cd at a lower dose level only in subjects with hypertensive heredity. Depression in systolic blood pressure may be a sign of Cd toxicity.2) Both normotensive and spontaneously hypertensive rats were given 15 g/day pelleted food containing PbCl_2 at a dose level of 0,3,30 or 300 ppm. Age-related elevation in systolic blood pressure was accelerated only in SHR rats exposed to 3 ppm Pb. This might suggest that systolic blood pressure is accelerated by Pb at a lower dose level only in subjects with hypertensive heredity. Supplemental studies suggested that age-related elevation in systolic blood pressure was accelerated more markedly by Pb at lower dose levels (0.3 and 1 ppm), and that blood pressure elevation may be accelerated by atherosclerosis through abnormal cholesterol metabolism.3) Both normotensive and spontaneously hypertensive rats were given 15 g/day pelleted food containing HgCl_2 at a dose level of 0,1,3 10 or 30 ppm. Age-related elevation in systolic blood pressure was accelerated only in SHR rats exposed to all levels of Hg. Biochemical data suggested that age-related elevation in systolic blood pressure may be accelerated by atherosclerosis through abnormal cholesterol metabolism induce by Hg.