Many studies indicate that blood pressure control systems can attenuate pai
n (hypoalgesia) of short duration; however, we recently found exaggerated n
ociceptive responses (hyperalgesia) of persistent duration in the spontaneo
usly hypertensive rat (SHR). Here, we used SHR, Dahl Salt-Sensitive (SS), a
nd normotensive control rats to evaluate the contribution of sustained elev
ations in arterial pressure to nociceptive responses. Compared with Sprague
-Dawley and/or Wistar-Kyoto controls, SHR were 1) hypoalgesic in the hot pl
ate test and 2) hyperalgesic in longer latency tail and paw-withdrawal test
s and in two models of inflammatory nociception. These differences were not
observed between SS and salt-resistant controls fed a high-salt diet. Infl
ammatory 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 p
ressure and not to sustained elevations in blood pressure, differences in s
pinal neuron activity, or inflammatory edema.