医学
交感神经系统
阻塞性睡眠呼吸暂停
内科学
肾上腺素
血压
内分泌学
去甲肾上腺素
高血压的病理生理学
唤醒
肥胖
睡眠呼吸暂停
心理学
神经科学
多巴胺
作者
Michael G. Ziegler,Milos Milic
出处
期刊:Current Opinion in Nephrology and Hypertension
[Ovid Technologies (Wolters Kluwer)]
日期:2016-10-16
卷期号:26 (1): 26-30
被引量:23
标识
DOI:10.1097/mnh.0000000000000288
摘要
The sympathetic nervous system (SNS) mediates short-term increases in blood pressure. Evidence that psychosocial stress leads to chronic hypertension is mixed. The SNS activation found in obstructive sleep apnea (OSA), caregiving for a severely demented spouse, and obesity more specifically address whether SNS activation might lead to the metabolic syndrome and hypertension.Obesity is associated with both increased SNS electrical activity and plasma norepinephrine. This is partly because of frequent OSA among the obese, but OSA does not fully explain SNS activation in obesity. Large stresses activate adrenal epinephrine release, but both animal and human studies indicate that epinephrine decreases aspects of the metabolic syndrome. On the other hand, norepinephrine is chronically elevated in OSA and among markedly stressed caregivers, and they have an increased incidence of hypertension. This is most striking in OSA, which causes a nocturnal diuresis. Hypertensive patients with OSA are resistant to the antihypertensive effects of diuretics, but respond to drugs that block SNS activity and the effects of renin.The SNS may mediate chronic blood pressure increases in response to specific stresses and alter responses to therapy. Evidence linking psychosocial stress to hypertension is mixed.
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