Taylor B K, Roderick R E, St Lezin E, Basbaum A I
Division of Pharmacology, School of Pharmacy, University of Missouri-Kansas City, Kansas City, Missouri 64108, USA.
Am J Physiol Regul Integr Comp Physiol. 2001 Feb;280(2):R345-54. doi: 10.1152/ajpregu.2001.280.2.R345.
Many studies indicate that blood pressure control systems can attenuate pain (hypoalgesia) of short duration; however, we recently found exaggerated nociceptive responses (hyperalgesia) of persistent duration in the spontaneously hypertensive rat (SHR). Here, we used SHR, Dahl Salt-Sensitive (SS), and normotensive control rats to evaluate the contribution of sustained elevations in arterial pressure to nociceptive responses. Compared with Sprague-Dawley and/or Wistar-Kyoto controls, SHR were 1) hypoalgesic in the hot plate test and 2) hyperalgesic in longer latency tail and paw-withdrawal tests and in two models of inflammatory nociception. These differences were not observed between SS and salt-resistant controls fed a high-salt diet. Inflammatory hyperalgesia in SHR was correlated with neither paw edema nor the number of Fos-positive spinal cord neurons. Our results indicate that "pain" phenotype of the SHR is not restricted to hypoalgesia. This phenotype is related to genetic factors or to the autonomic systems that control blood pressure and not to sustained elevations in blood pressure, differences in spinal neuron activity, or inflammatory edema.
许多研究表明，血压控制系统可减轻短期疼痛（痛觉减退）；然而，我们最近在自发性高血压大鼠（SHR）中发现了持续时间较长的痛觉过敏反应（痛觉过敏）。在此，我们使用SHR、Dahl盐敏感（SS）大鼠和正常血压对照大鼠来评估动脉血压持续升高对伤害性反应的影响。与Sprague-Dawley和/或Wistar-Kyoto对照相比，SHR在热板试验中表现为1）痛觉减退，在较长潜伏期的尾部和爪部撤离试验以及两种炎症性伤害感受模型中表现为2）痛觉过敏。在高盐饮食喂养的SS大鼠和抗盐对照大鼠之间未观察到这些差异。SHR中的炎症性痛觉过敏与爪部水肿或Fos阳性脊髓神经元数量均无相关性。我们的结果表明，SHR的“疼痛”表型并不局限于痛觉减退。这种表型与遗传因素或控制血压的自主神经系统有关，而与血压持续升高、脊髓神经元活动差异或炎症性水肿无关。
