Hypertension, Vol 5, 185-190, Copyright © 1983 by American Heart Association
JM Sitsen and W de Jong
In this study a possible relationship between regulatory mechanisms
involved in pain and blood pressure control has been investigated in the
rat. Spontaneously hypertensive rats (SHR), their normotensive Wistar-Kyoto
(WKY) controls, and two experimental models of hypertension together with
their appropriate sham-operated controls were tested for their
responsiveness to pain. Two methods for measurement of nociceptive
responsiveness (hot plate and electric footshock threshold) were used. A
diminished responsiveness was observed in both young (still normotensive)
and adult (hypertensive) SHR. Pretreatment with naloxone reduced hot plate
response times of adult SHR to the level of WKY, indicating opioid receptor
involvement. Despite severe hypertension in rats with a renal artery clip
and in DOCA-salt treated rats, no reduction of pain sensitivity as compared
to sham-operated controls was evident in the hypertensive rats as assessed
by both methods. It is concluded, that the higher pain threshold in SHR is
probably determined by genetic factors rather than hypertension.
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Hypoalgesia in genetically hypertensive rats (SHR) is absent in rats with experimental hypertension
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