Yamamoto I, Morimoto S, Uchida K, Hosojima H, Kakita T, Kigoshi T, Azukizawa S
Endocrinol Jpn. 1982 Dec;29(6):725-31. doi: 10.1507/endocrj1954.29.725.
A 37-year-old woman with postoperative hypoparathyroidism had hypertension, and elevated plasma renin activity (PRA) and subsequent hyperaldosteronism during a two-month hypercalcemic period caused by vitamin D and excessive calcium supplements. The hypertension with elevated PRA, however, was resistant to the angiotensin II (AII) analog [Sar1, Ile8] ALL. PRA further increased and plasma aldosterone decreased in response to the [Sar1, Ile8] ALL. When the patient became normocalcemic, normotensive and normoreninemic, calcium gluconate (5 mg calcium/kg/h) was infused for one hour. The calcium infusion reproduced hypercalcemic hypertension mediated by an increase in total peripheral resistance. These observations suggest that the hypertension observed while taking vitamin D and excessive calcium supplements may be caused by a direct effect of calcium on peripheral blood vessels and the renin-angiotensin system may play a negligible role.
一名37岁患有术后甲状旁腺功能减退的女性,在因维生素D和过量补钙导致的两个月高钙血症期间出现高血压、血浆肾素活性(PRA)升高及随后的醛固酮增多症。然而,PRA升高的高血压对血管紧张素II(AII)类似物[Sar1,Ile8]ALL耐药。给予[Sar1,Ile8]ALL后,PRA进一步升高而血浆醛固酮降低。当患者血钙、血压和肾素水平恢复正常时,静脉输注葡萄糖酸钙(5mg钙/kg/h)1小时。钙输注再现了由总外周阻力增加介导的高钙血症性高血压。这些观察结果表明,服用维生素D和过量补钙时观察到的高血压可能是钙对外周血管的直接作用所致,而肾素-血管紧张素系统可能起的作用微不足道。