Participation of AT1 and Mas receptors in the modulation of inflammatory pain.

We investigated the mechanisms underlying the endogenous control of nociception at the peripheral level during inflammation. We hypothesized that angiotensin receptors could modulate pain at the peripheral level via endogenous processes because angiotensin receptors are present in peripheral nerve terminals. We evaluated the role of the angiotensin receptors system (RAS) in the modulation of inflammatory and neuropathic pain states. Mas receptor KO mice exhibited major inflammatory pain compared to wild-type mice. Similar results were observed when rats were injected with the Mas receptor antagonist A779 or the AT1 receptor antagonist, losartan after inflammatory stimulation by carrageenan. However, these antagonists were not effective in animals with neuropathic-induced pain (e.g., sciatic nerve constriction). Therefore, RAS seems to play an important role in inflammatory but not neuropathic pain.

Assay of therapeutic ultrasound induced-antinociception in experimental trigeminal neuropathic pain.

Trigeminal neuralgia is considered one of the most painful conditions, and pharmacological treatment can be as debilitating as the pathology itself. The aim of this work was to evaluate the effectiveness of pulsed therapeutic ultrasound (TU) on an experimental rat model of trigeminal neuropathic nociception (chronic constriction injury-infraorbital nerve; CCI-ION). To evaluate facial thermonociception, an apparatus that measured the reaction time for head withdrawal was constructed. After surgery, a gradual reduction in reaction time was observed until day 15 post-CCI, when the values became constant. Three ipsilateral applications of TU to post-CCI rats promoted an increase in latency time. This antinociceptive effect was evident even after the first TU application, reaching maximal values at 24 hr. The magnitude of this effect was proportional to ultrasonic wave intensity (0.3 and 0.4 W/cm(2)). Posttreatment with naltrexone (5 mg/kg, s.c.) completely blocked the hypoalgesic effect of TU. Pretreatment with an opioid antagonist was unable to block the antinociceptive effect during the first 8 hr, suggesting that opioids are involved only in the latter phase of the TU effects. Myeloperoxidase (MPO) levels in the infraorbital nerve were not increased by TU use, indicating that TU causes no injury or is at least insufficient to induce neutrophil migration. In conclusion, TU is an effective resource in a model of trigeminal neuropathic pain, with a mechanism involving opioid receptor activation, confirming its potential usefulness in the treatment of trigeminal neuralgia.