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原发性高血压患者甲状旁腺功能增强:对尿钙流失的一种稳态反应。

Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak.

作者信息

McCarron D A, Pingree P A, Rubin R J, Gaucher S M, Molitch M, Krutzik S

出版信息

Hypertension. 1980 Mar-Apr;2(2):162-8. doi: 10.1161/01.hyp.2.2.162.

DOI:10.1161/01.hyp.2.2.162
PMID:7380520
Abstract

Disorders of calcium metabolism are not generally considered important either clinically or pathophysiologically in essential hypertension. Recent reports, though, suggest that increased parathyroid gland function may be one of the more common endocrine disturbances associated with hypertension. We measured serum parathyroid hormone (PTH) concentrations as well as routine blood and urine chemistries in 34 hypertensives. Their mean PTH, 79.1 +/- 3.1 muliter Eq/muliter, was significantly higher (p less than 0.025) than the mean PTH, 66.9 +/- 3.3, of an age- and sex-matched normotensive control population. The mean serum calcium, 9.5 +/- 0.1 mg%, was identical in the two populations. Compared to a second age- and sex-matched normotensive population, the hypertensives demonstrated a significant (p less than 0.005) relative hypercalciuria. For any level of urinary sodium, hypertensives excreted more calcium. These preliminary data suggest that parathyroid gland function may be enhanced in essential hypertension. This increased gland activity appears, in part, to be an appropriate, physiologic response to a previously unrecognized relative hypercalciuria, or renal calcium leak, associated with essential hypertension. We conclude that the increased prevalence of hypertension in subjects with hyperparathyroidism probably represents the final event in a continuum that begins with obligatory urinary calcium losses in hypertensives, but whose pathological presentation is hyperparathyroidism. The results of this pilot study indicate a need for derivative experiments directed at defining the importance of our preliminary findings in the pathogenesis of human and experimental hypertension.

摘要

钙代谢紊乱在原发性高血压中,无论是临床还是病理生理方面,一般都不被认为是重要的。然而,最近的报告表明,甲状旁腺功能增强可能是与高血压相关的较为常见的内分泌紊乱之一。我们测定了34名高血压患者的血清甲状旁腺激素(PTH)浓度以及常规血液和尿液化学成分。他们的平均PTH为79.1±3.1皮摩尔当量/毫升,显著高于年龄和性别匹配的正常血压对照人群的平均PTH(66.9±3.3)(p<0.025)。两组人群的平均血清钙均为9.5±0.1毫克%。与另一组年龄和性别匹配的正常血压人群相比,高血压患者表现出显著的(p<0.005)相对高钙尿症。对于任何尿钠水平,高血压患者排出的钙更多。这些初步数据表明,原发性高血压患者的甲状旁腺功能可能增强。这种腺体活性增加似乎部分是对原发性高血压相关的先前未被认识到的相对高钙尿症或肾钙泄漏的一种适当的生理反应。我们得出结论,甲状旁腺功能亢进患者中高血压患病率增加可能代表了一个连续过程的最终事件,这个过程始于高血压患者必然的尿钙流失,但其病理表现为甲状旁腺功能亢进。这项初步研究的结果表明需要进行进一步的实验,以确定我们的初步发现在人类和实验性高血压发病机制中的重要性。

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Enhanced parathyroid function in essential hypertension: a homeostatic response to a urinary calcium leak.原发性高血压患者甲状旁腺功能增强:对尿钙流失的一种稳态反应。
Hypertension. 1980 Mar-Apr;2(2):162-8. doi: 10.1161/01.hyp.2.2.162.
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Effect of saline infusion on urinary calcium excretion in essential hypertension.盐水输注对原发性高血压患者尿钙排泄的影响。
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