Doris P A, Harvey S, Pang P K
Life Sci. 1987 Sep 14;41(11):1383-9. doi: 10.1016/0024-3205(87)90613-8.
Plasma parathyroid hormone (pPTH) levels have been assessed in three separate radioimmunoassay systems in samples from Wistar-Kyoto rats. The animals were subjected to one of three dietary regimens throughout the study period: Group 1 animals consumed normal rat chow and drank tap water; Group 2 animals consumed normal rat chow and tap water was replaced with 0.5% saline solution; Group 3 animals consumed normal rat chow to which 2.5% CaCO3 (by weight) had been added and also drank 0.5% saline solution. Animals had consumed these diets for approximately 7 months prior to sacrifice for blood collection. Blood pressure was measured by tail cuff plethysmography in these animals and, as previously reported, saline consuming animals showed a moderate hypertension (Gp 2) only when diets did not contain added calcium (Gp 3). In the week prior to sacrifice, mean blood pressures were: Gp 1: 128.0 +/- 3.46 mmHg; Gp 2: 140.2 +/- 3.15 mmHg; and Gp 3: 133.5 +/- 2.90 mmHg. Three assay systems were used to measure pPTH levels from trunk blood samples obtained by guillotine decapitation. One assay used an antiserum directed toward the vasoactive N terminal fragment 1-34 and produced pPTH measurements of 0.74 +/- 0.05 ng/ml in Gp 1 animals, 1.04 +/- 0.07 ng/ml in Gp 2 animals and 1.12 +/- 0.08 ng/ml in Gp 3 animals. This pattern was consistent with that obtained by another antiserum which had been raised against the intact 1-84 PTH molecule and produced values of 0.25 +/- 0.03 ng/ml in Gp 1 animals, 0.55 +/- 0.07 ng/ml in Gp 2 animals and 0.74 +/- 0.04 ng/ml in Gp 3 animals. Antiserum raised against the C-terminal did not show any difference in pPTH across groups. We conclude that saline consumption may increase some portions of circulating PTH. Such elevation of pPTH may not be a pathophysiological component in the sodium dependent elevation of blood pressure since animals concurrently consuming both saline and calcium supplemented diets retained elevated pPTH levels even though blood pressures did not differ from controls. Rather, elevation of circulating PTH levels may be a response to prolonged increases in sodium consumption.
在来自Wistar - Kyoto大鼠的样本中，已在三种不同的放射免疫分析系统中评估了血浆甲状旁腺激素（pPTH）水平。在整个研究期间，动物接受三种饮食方案之一：第1组动物食用正常大鼠饲料并饮用自来水；第2组动物食用正常大鼠饲料，自来水被0.5%盐溶液替代；第3组动物食用添加了2.5%碳酸钙（按重量计）的正常大鼠饲料，并且也饮用0.5%盐溶液。在处死动物采集血液之前，动物已食用这些饮食约7个月。通过尾袖体积描记法测量这些动物的血压，并且如先前报道的那样，仅当饮食中不添加钙时（第3组），饮用盐溶液的动物才表现出中度高血压（第2组）。在处死前一周，平均血压分别为：第1组：128.0±3.46 mmHg；第2组：140.2±3.15 mmHg；第3组：133.5±2.90 mmHg。使用三种分析系统测量通过断头台斩首获得的躯干血样本中的pPTH水平。一种分析使用针对血管活性N末端片段1 - 34的抗血清，在第1组动物中测得的pPTH为0.74±0.05 ng/ml，在第2组动物中为1.04±0.07 ng/ml，在第3组动物中为1.12±0.08 ng/ml。这种模式与另一种针对完整的1 - 84 PTH分子产生的抗血清所获得的模式一致，在第1组动物中该抗血清测得的值为0.25±0.03 ng/ml，在第2组动物中为0.55±0.07 ng/ml，在第3组动物中为0.74±0.04 ng/ml。针对C末端产生的抗血清在各组之间未显示出pPTH有任何差异。我们得出结论，饮用盐溶液可能会增加循环中PTH的某些部分。pPTH的这种升高可能不是钠依赖性血压升高的病理生理成分，因为同时食用盐溶液和补钙饮食的动物即使血压与对照组无差异，其pPTH水平仍保持升高。相反，循环中PTH水平的升高可能是对钠摄入量长期增加的一种反应。
