![]() ![]() We demonstrate how CB 1 agonism or antagonism can modulate arthritic disease. ![]() In this review, we focus on CB 1 and transient receptor potential vanilloid 1 (TRPV1)-mediated effects on RA since most anti-inflammatory mechanisms induced by cannabinoids are attributed to cannabinoid receptor type 2 (CB 2) activation. In addition, many cell types in synovial tissue express CB 1 and TRPs. TRPs not only induce the sensation of pain but also support inflammation via secretion of pro-inflammatory neuropeptides. These ECs also modulate function of transient receptor potential channels (TRPs) located on sensory nerve fibers, which are abundant in arthritic synovial tissue. Peripheral norepinephrine release from sympathetic terminals is controlled by cannabinoid receptor type 1 (CB 1), which is activated by two major endocannabinoids (ECs), arachidonylethanolamine (anandamide) and 2-arachidonylglycerol. Several animal models of arthritis already demonstrated a profound influence of adrenergic signaling on the course of RA. ![]() Chronic inflammation in rheumatoid arthritis (RA) is accompanied by activation of the sympathetic nervous system, which can support the immune system to perpetuate inflammation. ![]()
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