| Research Abstract |
The aim of this study was to explore whether renin-angiotensin axix associates neuropathic pain. ACE gene polymorphism (DD and II homozygotes, and ID heterozygotes) associates the genetic risk factor for neuropathic pain. The distribution of the DD, ID and II genotypes in the study group is 33%, 33% and 33%, respectively. ACE activity was significantly higher in subjects with the ACE DD genotype than subjects with the ID and H genotypes. No significant difference in heart rate and blood pressure variabilities, plasma renin activity, angiotensin I and II was detected among the ACE genotypes. The frequency of the ACE DD genotype in the present population (33%) was higher than those previously described in other normal populations of the same race (20%).3 In addition, the frequency of the ACE DD genotype in CRPS type I was higher than those in CRPS type II
It is possible that the DD genotype favors the development of neuropathic pain as well as cardiovascular disease, perhaps through the p
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resence of higher ACE concentrations. Elevated ACE activity in these subjects may result in increased angiotensin n levels in the effector site, and this might be a mechanism underlying the association between the ACE deletion polymorphism and the increased genetic risk for susceptibility to neuropathic pain. Typing for ACE I/D gene poly-morphism, thus, might be a useful predictor of neuropathic pain.Aim of Investigation : Increased nociceptive thresholds have been reported in hypertensive rats and humans. Spontaneous hypertensive rats (SHR) have been known to have increased sympathetic tones which might alter the peripheral mononeuropathy. To test this hypothesis, we measured peripheral nerve injury-induced heat allodynia in SHR.
Methods : Chronic constrictive injury (CCI) was produced by loosely ligation of the unilateral sciatic nerve in normotensive Sprague-Dawely (SD) rat and SHR. The magnitude of the hyperesthesia was evaluated with the difference score (DS) which was the result of subtracting the latency of the withdrawal reflex on the control (sham-operated) side from the latency on the nerve injured side to the radiant heat stimulation. Systolic blood pressure (SBP) was oscillometrically measured. Data were expressed as meanアSEM, and analyzed by ANOVA. P<0.05 was considered significant.
Results : SD rats undergoing CCI showed decrease in DS from 0.85【minus-plus】0.39 before CCI to 1.67【minus-plus】1.12, -2.51【minus-plus】2.07 and -0.63【minus-plus】0.83, 4, 7 and 14days after CCI, respectively. On the contrary, DS hi SHR unchanged throughout the measurement, from -1.58【minus-plus】0.87 before CCI to 0.2【minus-plus】0.49, -0.85【minus-plus】0.83 and -1.95【minus-plus】1.02, 4, 7 and 14days after CCI, respectively.SBP before CCI were 126【minus-plus】8 (SD) and 177【minus-plus】6 (SHR).
Conclusions : SHR have been reported to have decreased sensitivity to pain, but as yet a mechanism has not been identified. CCI model hi SHR caused a reduction hi thermal hyperalgesia, indicating that a genetic predisposition to hypertension may attenuate the mononeuropathic thermal hyperlgesia Less
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