Peripheral nitric oxide signaling directly blocks inflammatory pain

Author(s)

Gomes, Francisco Isaac F. ; Cunha, Fernando Q. ; Cunha, Thiago M.

• Document type: Journal article
• Source: Biochemical Pharmacology; v. 176, p. 11-pg., 2020-06-01.

Abstract

Pain is a classical sign of inflammation, and sensitization of primary sensory neurons (PSN) is the most important mediating mechanism. This mechanism involves direct action of inflammatory mediators such as prostaglandins and sympathetic amines. Pharmacologic control of inflammatory pain is based on two principal strategies: (i) non-steroidal anti-inflammatory drugs targeting inhibition of prostaglandin production by cyclooxygenases and preventing nociceptor sensitization in humans and animals; (ii) opioids and dipyrone that directly block nociceptor sensitization via activation of the NO signaling pathway. This review summarizes basic concepts of inflammatory pain that are necessary to understand the mechanisms of peripheral NO signaling that promote peripheral analgesia; we also discuss therapeutic perspectives based on the modulation of the NO pathway. (AU)

• FAPESP's process: 13/08216-2 - CRID - Center for Research in Inflammatory Diseases
• Grantee: Fernando de Queiroz Cunha
• Support Opportunities: Research Grants - Research, Innovation and Dissemination Centers - RIDC
• FAPESP's process: 19/14285-3 - Role of succinate/SUCNR1 signalling pathway in sensory neurons in neuropathic pain development
• Grantee: Francisco Isaac Fernandes Gomes Aragão
• Support Opportunities: Scholarships in Brazil - Doctorate