McCubbin J A, Surwit R S, Williams R B
Department of Psychiatry, Duke University Medical Center, Durham, NC 27710.
Psychosom Med. 1988 Jan-Feb;50(1):8-14. doi: 10.1097/00006842-198801000-00002.
Opioidergic inhibition of sympathetic nervous system responses may be deficient in persons at risk for essential hypertension (McCubbin et al: Hypertension 7:808, 1985). The opiate antagonist naloxone increases blood pressure responses during psychological stress in young adults with low causal blood pressure, but has no pressor effect in subjects with high casual blood pressure. The purpose of the present study was to determine the role of altered baroreflex function in the abnormal pressor effect of naloxone in persons at risk for hypertension development. We tested this by comparison of the effects of naloxone on responses to psychological stress with responses to orthostatic stress in persons with high and low casual blood pressure. The results suggest that abnormal opioidergic control of systolic blood pressure responses to psychological stress is not likely a result of altered baroreflex function. Persons at risk for hypertension show evidence of an opioid peptide lesion that can probably be localized either at the adrenal medullae or at levels of central autonomic control that are parallel with or rostral to baroreflex circuits.
阿片能对交感神经系统反应的抑制在原发性高血压风险人群中可能存在缺陷（麦库宾等人：《高血压》7:808，1985年）。阿片拮抗剂纳洛酮会增加血压正常的年轻成年人在心理应激期间的血压反应，但对血压正常偏高的受试者没有升压作用。本研究的目的是确定压力反射功能改变在纳洛酮对高血压发生风险人群的异常升压作用中的作用。我们通过比较纳洛酮对血压正常偏高和正常偏低的人心理应激反应与直立应激反应的影响来对此进行测试。结果表明，对心理应激的收缩压反应的阿片能控制异常不太可能是压力反射功能改变的结果。高血压风险人群显示出阿片肽损伤的证据，这种损伤可能定位于肾上腺髓质或与压力反射回路平行或位于其上方的中枢自主控制水平。
