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Am J Physiol Regul Integr Comp Physiol 280: R345-R354, 2001;
0363-6119/01 $5.00
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Vol. 280, Issue 2, R345-R354, February 2001

Hypoalgesia and hyperalgesia with inherited hypertension in the rat

Bradley K. Taylor1, Robyn E. Roderick2, Elizabeth St. Lezin3, and Allan I. Basbaum2

1 Division of Pharmacology, School of Pharmacy, University of Missouri-Kansas City, Kansas City, Missouri 64108; 2 W. M. Keck Foundation Center for Integrative Neuroscience and Departments of Anatomy and Physiology and 3 Laboratory Medicine, University of California San Francisco, San Francisco, California 94143

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.

pain; inflammation; Dahl salt-sensitive rat; spontaneously hypertensive rat


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