DIETARY CALCIUM INDUCES REGRESSION OF LEFT-VENTRICULAR HYPERTROPHY IN HYPERTENSIVE NON-INSULIN-DEPENDENT DIABETIC BLACKS

被引:26
作者
ZEMEL, MB
ZEMEL, PC
BRYG, RJ
SOWERS, JR
机构
[1] Divisions of Endocrinology and Cardiology, Department of Nutrition and Food Science, Wayne State University, Detroit, MI
[2] Veterans Administration Medical Center, Allen Park, MI
关键词
Blacks; Calcium; Left ventricular hypertrophy; Vascular resistance;
D O I
10.1093/ajh/3.6.458
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Recent data from this laboratory indicate that dietary calcium supplementation causes reduced in-tracellular calcium in type II diabetic hypertensives. Consequently, we have assessed the effects of calcium supplementation on forearm blood flow (FBF) and vascular resistance (FVR) and left ventricular mass (LVM) in seven type II diabetic hypertensive black men with left ventricular hypertrophy (LVH) maintained off antihypertensive treatment for four weeks and then supplemented with 600 mg calcium per day for three months. A comparable group of black diabetic hypertensive patients treated with atenolol (50 mg) served as controls. LVM was determined by M-mode echocardiography and FBF and FVR by electrical impedance plethysmography at the end of the four week baseline and the 12 week supplementation periods. Calcium supplementation resulted in a decrease (P <.05) in mean arterial pressure (from 121 ± 4 to 114 ± 3 mm Hg) which was accompanied by an 18% increase in FBF and a 20% reduction in FVR (P <.05). LVM decreased from 289 ± 22 at baseline to 240 ± 22 g at the end of the supplementation period (P <.02) and there was a significant correlation between changes in FBF and LVM (r = 0.82). Left ventricular end diastolic dimension decreased by 11% (P <.05). These data indicate that calcium supplementation sufficient to normalize dietary calcium in black hypertensive diabetic men significantly reduces vascular resistance and causes partial regression of LVH. Am J Hyper-tens 1990;3:458-463. © 1990, American Journal of Hypertension, Ltd. All rights reserved.
引用
收藏
页码:458 / 463
页数:6
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