This review focused on how transient receptor potential vanilloid 1, endothelin-1/endothelin type A receptor, and cannabinoid receptors contributed to the pathophysiology of SCD-associated pain.
Over the years various treatment modalities have been tried and tested to improve the pain management including the use of non-steroidal anti-inflammatory drugs (NSAIDs), opioids, bisphosphonates, tricyclic antidepressants, corticosteroids, growth factors and signaling molecules, ET-1 receptor antagonists, radiotherapy as well as surgical management.
Elevated levels of plasma TNF-α, IL-8, and ET-1 further establish the chronic inflammatory state in SCA and equally affirm their significant contribution, not only to pathogenesis but also to the severity of pain in SCA.
The present study demonstrated (1) the presence and the function of the BK system in endometriosis, (2) activation of BKR induced endothelin-1 in endometriotic lesion and (3) blocking endothelin-1 was effective to decrease pain.
Recent studies in our laboratory have revealed that low-level blast exposure increased expression of transient receptor potential vanilloid 1 (TRPV1) and endothelin-1 (ET-1), proteins well characterized for their role in mediating pain transmission, in the cornea.
The present study investigated whether endothelin-1 acts via ET<sub>A</sub> or ET<sub>B</sub> receptors to mediate superoxide anion-induced pain and inflammation.
The present study assessed the effects of ETBR activation and the role of endogenous opioid analgesia in carcinoma pain using an orthotopic cancer pain mouse model. mRNA expression analysis showed that ET-1 was nearly doubled while ETBR was significantly down-regulated in a human oral SCC cell line compared to normal oral keratinocytes (NOK).
Role of ET(A) and ET(B) endothelin receptors on endothelin-1-induced potentiation of nociceptive and thermal hyperalgesic responses evoked by capsaicin in rats.