Schleiffer R
Biologie Cellulaire & Physiopathologie Digestives, INSERM U61, Strasbourg, France.
Int J Cardiol. 1992 Jun;35(3):303-10. doi: 10.1016/0167-5273(92)90227-t.
Recent research provides evidence that parathyroid hormone is implicated in the pathogenesis of genetic hypertension. Abnormalities in calcium metabolism in genetic hypertension have been reported. These include hypercalciuria, depressed serum ionized calcium associated with enhanced serum parathyroid hormone levels. Calcium supplement resulted in normalization of calcium metabolism and reduction in blood pressure. In addition, removal of parathyroid glands attenuated the rise in blood pressure in genetic hypertensive rat. This review focuses on the links between calcium metabolism and calcium endocrine system abnormalities and the etiology of experimental genetic hypertension. The mechanisms by which dietary supplement and parathyroidectomy lower genetic hypertension are also discussed. Although the causality of raised parathyroid hormone in genetic hypertension is not yet fully understood, we conclude that this hormone may play a permissive effect in the development of hypertension.
近期研究表明甲状旁腺激素与遗传性高血压的发病机制有关。已有报道称遗传性高血压患者存在钙代谢异常。这些异常包括高钙尿症、血清离子钙降低以及血清甲状旁腺激素水平升高。补充钙剂可使钙代谢恢复正常并降低血压。此外，切除甲状旁腺可减轻遗传性高血压大鼠的血压升高。本综述重点关注钙代谢与钙内分泌系统异常之间的联系以及实验性遗传性高血压的病因。同时也讨论了膳食补充剂和甲状旁腺切除术降低遗传性高血压的机制。尽管甲状旁腺激素升高在遗传性高血压中的因果关系尚未完全明确，但我们得出结论，这种激素可能在高血压的发生发展中起促进作用。
