Williams R R, Hopkins P N
Prog Clin Biol Res. 1979;32:183-94.
Observations relating to hypertension in humans and rat experiments have been reviewed from several viewpoints including clinical medicine, pathophysiology, epidemiology, and genetics. It seems likely that much of essential hypertension results from excessive salt intake by individuals with an inherited inability to excrete sodium efficiently which is compensated by blood pressure elevation. A few major genes are likely responsible for a few basic mechanisms involving renal membranes and hormones controlling sodium transport. Excess hypertension in blacks, diabetics, the elderly, and oral contraceptive users can be explained by this theory. If hypertension and other genetically predisposed CHD risk factors are to be fully understood, future studies are needed with detailed data on both genetic and environmental factors, and analytic tools that allow an adequate examination of their interactions.
已从临床医学、病理生理学、流行病学和遗传学等多个角度对人类高血压及大鼠实验的相关观察进行了综述。原发性高血压很可能是由个体遗传性排钠功能障碍导致盐摄入过多引起的,而这会通过血压升高来代偿。一些主要基因可能与涉及肾膜及控制钠转运的激素的几种基本机制有关。黑人、糖尿病患者、老年人及口服避孕药使用者中过高的高血压发病率可用该理论解释。若要全面理解高血压及其他遗传易感性冠心病危险因素,未来研究需要详细的遗传和环境因素数据以及能够充分检验它们相互作用的分析工具。