应激性高血压:“错误”环境中的“错误”基因。

G A Harshfield, C E Grim
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摘要

吉姆·亨利(Jim Henry)证明了动物社会可以诱发血压升高及其心血管疾病的后遗症。他认识到,升高血压所需的压力是受实验小鼠基因决定的行为特征的一种功能。他称一些菌株具有攻击性,另一些菌株具有和平性。作为高度近亲繁殖(实际上是等基因菌株),发现这些基因相同的个体一旦被置于一个领土减少的社会中,其行为会显著不同,这是很有趣的。一只占统治地位的“王”老鼠出现了。其他非支配性的雄性则具有侵略性,并努力成为国王。肾上腺髓质系统被激活,肾素升高。其他人挤在一个笼子里,似乎已经放弃了。吉姆称他们抑郁。肾上腺皮质增生提示垂体肾上腺轴与抑郁症一样激活,肾素水平低,皮质酮水平高。在大鼠中,必须谨慎选择具有侵略性基因的菌株,并结合社会压力的滴定,才能可靠地诱发高血压。人类很可能保留了一些(如果不是全部的话)这些变异,也就是说,一些人对压力的反应是血压升高,而另一些人则不会,一些人通过交感神经通路做出反应,另一些人通过肾上腺皮质激活做出反应。非裔美国人的高血压是由于压力引起的,这一建议与亨利范式和已知的遗传对黑人钠潴留的影响有关。本文提出并讨论了黑人饮食中钠对血压升高的遗传敏感性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Stress hypertension: the "wrong" genes in the "wrong" environment.

Jim Henry demonstrated an animal's society can induce an increase in blood pressure and its cardiovascular sequale. He recognized that the stress required to elevate blood pressure was a function of the genetically determined behavioral traits of the mice used. He termed some strains aggressive, others peaceable. Being highly inbred (indeed isogenic strains) it was intriguing to find that the behavior of these genetically identical individuals could differ markedly once placed in a society that decreased territory. A dominant or "king" mouse emerged. Other non-dominant males were aggressive and striving to be king. Adrenal medullary systems were activated and renins high. Others huddled in one cage and appeared to have given up. Jim called them depressed. Their adrenal cortex was hyperplastic suggesting pituitary adrenal axis activation as in depression, their renin was low and corticosterone high. In rats, careful selection of a strain genetically aggressive had to be combined with titration of societal stress to reliably induce hypertension. Its likely that humans retain some, if not all, of these variations, i.e. some respond to stress with an increase in blood pressure and others do not, some respond via the sympathetic pathway and others by adrenal cortical activation. The suggestion that African American's high blood pressures is due to stress is relevant to the Henry paradigm and the known genetic influences on sodium retention in blacks. The integration of this paradigm with the genetically increased sensitivity to the blood pressure raising effects of dietary sodium in blacks is proposed and discussed.

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