Weinberger M H, Miller J Z, Luft F C, Fineberg N S, Grim C E, Christian J C
Clin Exp Hypertens (1978). 1981;3(4):569-81. doi: 10.3109/10641968109033684.
Utilization of several genetic models (twins, families of monozygotic twins, characterized hypertensives and normotensive first-degree-relatives of essential hypertensives) has permitted us to probe for evidence of genetic mediation of several components of the blood pressure control system in humans. These studies have identified evidence for genetic mediation of systolic blood pressure in a cross-sectional study of normotensive subjects covering a wide age span. Further, this effect was independent of body size. The twin model, studied under conditions of sodium loading and sodium and volume depletion, demonstrated a genetic component in the response of plasma renin activity, aldosterone, norepinephrine and renal sodium excretion to these maneuvers. Among hypertensive subjects and unexpected abnormality in the distribution of a specific MNS blood group pattern was seen in renal vascular hypertensives. This may provide a new genetic marker for identifying individuals at increased risk to develop this abnormality.
利用几种遗传模型(双胞胎、同卵双胞胎家庭、确诊的高血压患者以及原发性高血压患者的血压正常的一级亲属),我们得以探究人类血压控制系统多个组成部分的遗传介导证据。这些研究在一项涵盖广泛年龄范围的血压正常受试者横断面研究中,确定了收缩压遗传介导的证据。此外,这种效应与体型无关。在钠负荷、钠和容量耗竭条件下进行研究的双胞胎模型表明,血浆肾素活性、醛固酮、去甲肾上腺素和肾钠排泄对这些操作的反应存在遗传成分。在高血压患者中,肾血管性高血压患者的特定MNS血型模式分布出现意外异常。这可能为识别发生这种异常风险增加的个体提供一种新的遗传标记。