Zamir N, Maixner W
Ann N Y Acad Sci. 1986;467:371-84. doi: 10.1111/j.1749-6632.1986.tb14641.x.
An increasing amount of anatomical, physiological, and pharmacological evidence suggest that pain inhibitory circuitry is linked with cardiovascular regulatory systems in man and laboratory animals. Induction of hypertension in rats by different methods (mineralocorticoid treatment, stenosis of renal artery, or social deprivation) is associated with reduced responsiveness to noxious thermal stimuli (hot-plate) or to noxious mechanical stimuli (paw pressure). Genetically hypertension-prone rats derived from the SABRA strain and spontaneously hypertensive rats derived from Wistar/Kyoto strain also display a similar hypoalgesia. Acute increases in blood pressure are associated with reduced sensitivity to painful stimuli. Additionally, the interaction between blood pressure and pain perception has also been supported by the demonstration that various experimental interventions that diminish the magnitude of hypertension also attenuate the hypoalgesia. Recent clinical findings are also in agreement with the laboratory animal findings since sensory and pain thresholds have been shown to be significantly higher in unmedicated essential hypertensive subjects compared to normotensive controls. Thus, the human data corroborate animal data and suggest that a relation between blood pressure and pain sensitivity is likely to be a general phenomenon. It is unlikely that damage to peripheral pain fibers caused by a change in blood pressure contributes to the observed hypoalgesia. Naloxone, which has no effect on blood pressure, returns the pain sensitivity to normal levels. Behavioral tests (open field and motor activity cage) of normotensive and of renal and genetically (SBH and SHR) hypertensive rats exclude the possibility of a general motor deficit in hypertensive rats. Endogenous opioid peptides in central and peripheral nervous systems as well as in endocrine organs are implicated, although non-opioid mechanisms are also evident. Activation of baroreceptor afferents by acute or chronic increases in arterial or venous blood pressure may play an important role in the somatosensory responses associated with the increase in blood pressure. Coordinated cardiovascular-pain regulatory responses may be part of an adaptive mechanism that helps the body to face stressful events.
越来越多的解剖学、生理学和药理学证据表明，在人类和实验动物中，疼痛抑制回路与心血管调节系统相关联。通过不同方法（盐皮质激素治疗、肾动脉狭窄或社会剥夺）诱导大鼠高血压，会导致对有害热刺激（热板）或有害机械刺激（爪部压力）的反应性降低。源自SABRA品系的遗传性高血压易患大鼠和源自Wistar/Kyoto品系的自发性高血压大鼠也表现出类似的痛觉减退。血压急性升高与对疼痛刺激的敏感性降低有关。此外，血压与疼痛感知之间的相互作用也得到了以下证据的支持：各种能降低高血压程度的实验干预措施也会减轻痛觉减退。最近的临床研究结果也与实验动物的研究结果一致，因为与血压正常的对照组相比，未经药物治疗的原发性高血压患者的感觉阈值和疼痛阈值明显更高。因此，人类数据证实了动物数据，并表明血压与疼痛敏感性之间的关系可能是一种普遍现象。血压变化导致外周疼痛纤维受损不太可能是观察到的痛觉减退的原因。对血压无影响的纳洛酮可使疼痛敏感性恢复到正常水平。对血压正常的大鼠以及肾性和遗传性（SBH和SHR）高血压大鼠进行的行为测试（旷场试验和运动活动笼试验）排除了高血压大鼠存在一般运动缺陷的可能性。中枢和外周神经系统以及内分泌器官中的内源性阿片肽被认为与此有关，尽管非阿片类机制也很明显。动脉或静脉血压急性或慢性升高激活压力感受器传入神经，可能在与血压升高相关的躯体感觉反应中起重要作用。心血管-疼痛调节反应的协调可能是一种适应性机制的一部分，有助于身体应对压力事件。
