STRESS HYPERTENSION - THE WRONG GENES IN THE WRONG ENVIRONMENT

Jim Henry demonstrated an animal's society can induce an increase in b lood pressure and its cardiovascular sequale. He recognized that the s tress required to elevate blood pressure was a function of the genetic ally determined behavioral traits of the mice used. He termed some str ains aggressive, others peaceable. Being highly inbred (indeed isogeni c strains) it was intriguing to find that the behavior of these geneti cally identical individuals could differ markedly once placed in a soc iety that decreased territory. A dominant or ''king'' mouse emerged. O ther non-dominant males were aggressive and striving to be king. Adren al medullary systems were activated and renins high. Others huddled in one cage and appeared to have given up. Jim called them depressed. Th eir adrenal cortex was hyperplastic suggesting pituitary adrenal axis activation as in depression, their renin was low and corticosterone hi gh. In rats, careful selection of a strain genetically aggressive had to be combined with titration of societal stress to reliably induce hy pertension. It;; likely that humans retain some, if not all, of these variations, i.e. some respond to stress with an increase in blood pres sure and others do not, some respond via the sympathetic pathway and o thers by adrenal cortical activation. The suggestion that African Amer ican's high blood pressures is due to stress is relevant to the Henry paradigm and the known genetic influences on sodium retention in black s. The integration of this paradigm with the genetically increased sen sitivity to the blood pressure raising effects of dietary sodium in bl acks is proposed and discussed.