Zemel M B, Bedford B A, Zemel P C, Marwah O, Sowers J R
Division of Endocrinology, Metabolism and Hypertension, Wayne State University, Detroit, Michigan 48202.
J Hypertens Suppl. 1988 Dec;6(4):S228-30. doi: 10.1097/00004872-198812040-00068.
Erythrocyte cation transport and intracellular calcium in 15 black type II diabetic hypertensives were compared with 11 otherwise similar non-diabetic hypertensives and 16 normal black adults. The diabetic hypertensives were then randomized into either a placebo group or a calcium-supplemented (600 mg/day) group and studied again after 4 weeks. Na+,K+-ATPase activity was significantly lower in both groups of hypertensives than in the normotensives. In contrast, Ca-ATPase activity was similar among the non-diabetic hypertensive and normotensives but was markedly (approximately 60%) suppressed in the diabetics, while intracellular calcium was proportionally elevated. Calcium supplements significantly increased Ca-ATPase activity and reduced intracellular calcium and blood pressure compared with the placebo group. We conclude that type II diabetes is characterized by a defect in Ca-ATPase which may be responsible for increases in intracellular calcium and vascular resistance and which is partially corrected by dietary calcium supplementation.
对15名患有II型糖尿病的黑人高血压患者的红细胞阳离子转运和细胞内钙水平，与11名其他情况相似的非糖尿病高血压患者以及16名正常黑人成年人进行了比较。然后将糖尿病高血压患者随机分为安慰剂组或补钙组（600毫克/天），4周后再次进行研究。两组高血压患者的钠钾ATP酶活性均显著低于血压正常者。相比之下，非糖尿病高血压患者和血压正常者的钙ATP酶活性相似，但糖尿病患者的钙ATP酶活性显著（约60%）受到抑制，而细胞内钙则相应升高。与安慰剂组相比，补钙显著提高了钙ATP酶活性，降低了细胞内钙水平和血压。我们得出结论，II型糖尿病的特征是钙ATP酶缺陷，这可能是细胞内钙和血管阻力增加的原因，而膳食补钙可部分纠正这一缺陷。
