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

ABSTRACT

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.