Kuchel Otto
University of Montreal, 34 Kenaston Avenue, Montreal, Quebec, Canada H3R 1L8.
J Hypertens. 2003 Mar;21(3):639-41. doi: 10.1097/01.hjh.0000052462.40108.fb.
Emotional stress acutely and repetitively causing blood pressure increase or aggravating existing hypertension is usually not reflected by norepinephrine and epinephrine increase but by a sudden rise of dopamine, the third "defensive" catecholamine coping with the damaging neuropsychological and cardiovascular actions of the first two. This double-edged sympathetic response to emotional stress evolves during human lifespan and long-term evolution of hypertension. In the course of philogenesis it carries a potential mismatch between the normal physiology of the human dopaminergic system and current environmental (emotional particularly) conditions in industrialized countries. This offers a rational support to a mental stress-cardiovascular diseases relationship proposed 40 years ago in a WHO report which followed a memorable 1960 Prague Hypertension Meeting.
情绪应激急性且反复地导致血压升高或加重现有的高血压,通常不是由去甲肾上腺素和肾上腺素的增加反映出来,而是由多巴胺的突然升高反映出来,多巴胺是应对前两者有害的神经心理和心血管作用的第三种“防御性”儿茶酚胺。这种对情绪应激的双刃剑式交感反应在人类生命周期和高血压的长期演变过程中逐渐形成。在种系发生过程中,它在工业化国家中人类多巴胺能系统的正常生理与当前环境(尤其是情绪)状况之间存在潜在的不匹配。这为40年前世界卫生组织的一份报告中提出的心理应激与心血管疾病的关系提供了合理的支持,该报告是在1960年令人难忘的布拉格高血压会议之后发布的。