Hypoalgesia in genetically hypertensive rats (SHR) is absent in rats with experimental hypertension.
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.
D000818:Animals; D004558:Electric Stimulation; D006358:Hot Temperature; D006973:Hypertension / Q000503:physiopathology*; D006977:Hypertension, Renal / Q000503:physiopathology; D008297:Male; D009619:Nociceptors / Q000503:physiopathology; D010146:Pain / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012684:Sensory Thresholds