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钙代谢与高血压

Calcium metabolism and hypertension.

作者信息

McCarron D A

机构信息

Oregon Health Sciences University, Portland.

出版信息

Kidney Int. 1989 Feb;35(2):717-36. doi: 10.1038/ki.1989.44.

Abstract

Returning to the patient presented today, perhaps we can now understand some of his findings. As I noted, men are more likely to demonstrate alterations in calcium metabolism associated with elevations in blood pressure. Furthermore, blacks are more likely than whites to develop hyperparathyroidism, particularly in the third and fourth decades of life. It is unlikely, however, that parathyroid hormone was responsible for the increase in this patient's arterial pressure because PTH has a vasodilating action. Moreover, the long-term response to parathyroidectomy is more likely to be an increase rather than a decrease in blood pressure. It is also unlikely that the mild elevations in the serum total calcium observed in this patient were responsible for his hypertension. Correction of hypercalcemia by surgical intervention failed to improve the blood pressure. There is little evidence that mild, protracted hypercalcemia can account for increases in arterial pressure. Finally, the patient's alcohol abuse might have contributed to his elevated blood pressure; it is possible that his hypertension was in part a reflection of the abnormal calcium metabolism he developed as a consequence of the alcohol abuse. Answers to some questions we faced when we first studied this patient more than a decade ago can be provided by the wealth of basic research and clinical investigation that has occurred since. We now know that calcium metabolism is a factor in blood pressure regulation in some humans and in some experimental models. Epidemiologic studies document a consistent association between lower dietary calcium intake and higher blood pressures in humans. An additional non-pharmacologic approach has been identified that can produce a modest but important lowering of blood pressure in a subset of hypertensive individuals. Much data show that calcium-regulating hormones have important cardiovascular actions that might account for some of the mechanisms by which increased dietary calcium lowers blood pressure. Research in this area also has set the stage for exploring another theoretical mechanism for sodium-chloride-sensitive hypertension. Finally, a theoretical mechanism(s) has emerged that could provide a pathophysiologic link between hypertension and certain high-risk populations such as blacks, the elderly, type-II diabetics, and pregnant women. The principal clinical implication derived from this work to date is the following: In patients with mild to moderate hypertension, the level of dietary calcium intake should be assessed. Patients whose intake is deficient should be encouraged simply to maintain calcium intake at 800 to 1000 mg/day.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

回到今天所介绍的这位患者,或许我们现在能理解他的一些检查结果了。如我所提到的,男性更有可能出现与血压升高相关的钙代谢改变。此外,黑人比白人更易患甲状旁腺功能亢进,尤其是在人生的第三个和第四个十年。然而,甲状旁腺激素不太可能是导致该患者动脉血压升高的原因,因为甲状旁腺激素具有血管舒张作用。而且,甲状旁腺切除术后的长期反应更可能是血压升高而非降低。该患者血清总钙轻度升高也不太可能是其高血压的病因。通过手术干预纠正高钙血症并未能改善血压。几乎没有证据表明轻度、持续性高钙血症可导致动脉血压升高。最后,该患者酗酒可能导致了他血压升高;他的高血压可能部分反映了因酗酒而出现的异常钙代谢。自十多年前我们首次研究这位患者以来所进行的大量基础研究和临床调查,能够为我们当时所面临的一些问题提供答案。我们现在知道,在一些人类个体和一些实验模型中,钙代谢是血压调节的一个因素。流行病学研究证明,人类饮食中钙摄入量较低与较高的血压之间存在持续的关联。已确定了另一种非药物方法,该方法可使一部分高血压患者的血压适度但显著降低。许多数据表明,钙调节激素具有重要的心血管作用,这可能解释了增加饮食钙摄入量可降低血压的部分机制。该领域的研究也为探索氯化钠敏感性高血压的另一种理论机制奠定了基础。最后,一种理论机制已经出现,它可能为高血压与某些高危人群(如黑人、老年人、II型糖尿病患者和孕妇)之间提供病理生理联系。迄今为止,这项研究的主要临床意义如下:对于轻度至中度高血压患者,应评估其饮食钙摄入量水平。摄入量不足的患者应被鼓励将钙摄入量维持在每日800至1000毫克。(摘要截选至400字)

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