Ferrari P, Weidmann P, Shaw S, Giachino D, Riesen W, Allemann Y, Heynen G
Medizinische Poliklinik, University of Bern, Switzerland.
Am J Med. 1991 Dec;91(6):589-96. doi: 10.1016/0002-9343(91)90211-f.
Essential hypertension is, in some patients, complicated by impairment of insulin-mediated glucose disposal and hyperinsulinemia. Whether this metabolic disturbance is a consequence of the hypertensive process or whether it may precede, and thus possibly promote, the development of hypertension has been unknown.
Searching for hereditary or familial defects in hypertension-prone humans, we prospectively investigated insulin sensitivity, plasma insulin and glucose, and serum lipoproteins in normotensive offspring of essential hypertensive as compared with age- and body habitus-matched offspring of normotensive families.
Compared with 78 control subjects, 70 offspring of essential hypertensive parents had similar age (mean +/- SEM: 24 +/- 1 versus 24 +/- 1 years, respectively) and body mass index (22.3 +/- 0.2 versus 22.4 +/- 0.2 kg/m2), a blood pressure of 127/77 +/- 1/1 versus 123/76 +/- 1/1 mm Hg (p less than 0.05 for systolic), and significantly elevated (p less than 0.01 to 0.001) fasting plasma insulin levels (9.9 +/- 0.3 versus 8.6 +/- 0.3 microU/mL), serum total triglycerides (1.03 +/- 0.06 versus 0.83 +/- 0.03 mmol/L), total cholesterol (4.37 +/- 0.08 versus 3.93 +/- 0.07 mmol/L), low-density lipoprotein cholesterol (2.45 +/- 0.08 versus 2.14 +/- 0.07 mmol/L), and total/high-density lipoprotein cholesterol ratio (4.3 +/- 0.1 versus 3.7 +/- 0.1). Insulin sensitivity was lower (9.4 +/- 0.7 versus 13.2 +/- 1.1 x 10(-4) x minute-1/microU/mL, p less than 0.001), while post-glucose-load plasma insulin levels were higher (p less than 0.05) in the 41 offspring of essential hypertensive parents than in the 38 offspring of normotensive parents so investigated.
These findings demonstrate that young normotensive humans in apparently excellent health but with one essential hypertensive parent tend to have an impairment of insulin-mediated glucose disposal, hyperinsulinemia, and dyslipidemia. It follows that a familial trait for essential hypertension seems to coexist commonly with defects in carbohydrate and lipoprotein metabolism that can be detected before or at least at a very early stage of the development of high blood pressure as judged by resting blood pressure measurements.
在一些患者中，原发性高血压并发胰岛素介导的葡萄糖代谢障碍和高胰岛素血症。这种代谢紊乱是高血压过程的结果，还是可能先于高血压发生并因此促进高血压的发展，一直尚不明确。
为了寻找高血压易感人群中的遗传或家族性缺陷，我们前瞻性地研究了原发性高血压患者的血压正常的后代与血压正常家族中年龄和体型匹配的后代的胰岛素敏感性、血浆胰岛素和葡萄糖以及血清脂蛋白。
与78名对照受试者相比，70名原发性高血压患者的后代年龄相仿（平均±标准误：分别为24±1岁和24±1岁），体重指数相当（22.3±0.2与22.4±0.2kg/m²），血压为127/77±1/1与123/76±1/1mmHg（收缩压p<0.05），空腹血浆胰岛素水平显著升高（p<0.01至0.001）（9.9±0.3与8.6±0.3μU/mL），血清总甘油三酯（1.03±0.06与0.83±0.03mmol/L）、总胆固醇（4.37±0.08与3.93±0.07mmol/L）、低密度脂蛋白胆固醇（2.45±0.08与2.14±0.07mmol/L）以及总胆固醇/高密度脂蛋白胆固醇比值（4.3±0.1与3.7±0.1）。在接受研究的41名原发性高血压患者的后代中，胰岛素敏感性较低（9.4±0.7与13.2±1.1×10⁻⁴×分钟⁻¹/μU/mL，p<0.001），而葡萄糖负荷后血浆胰岛素水平较高（p<0.05），高于38名血压正常的父母的后代。
这些发现表明，年轻的血压正常但有一位原发性高血压父母的人，往往存在胰岛素介导的葡萄糖代谢障碍、高胰岛素血症和血脂异常。由此可见，原发性高血压的家族性特征似乎通常与碳水化合物和脂蛋白代谢缺陷共存，这些缺陷在高血压发展之前或至少在通过静息血压测量判断的高血压发展的非常早期阶段就可以被检测到。
