Nevertheless the authors did not provide any pathophysiological substantiation of this effect. Probably, these changes were caused due to the antioxiodative features of capsaicin.
By the opinion of some authors the fact of capsaicin bidding to the intracellular side of the receptor is evidence of the presence of an endogenous intracellular activator. They consider that leukotrienes (products of LOs pathway of arachidocnic acid metabolism) could be such activator (ibid) (the hypothesis that certain products of LOs directly open capsaicin-activated channels. Thus the existence of the endogenous capsaicin-like substances was approved (Hwang et al., 2000; Huang et al., 2002).
5. Tominaga & Julius (2000) Capsaicin receptor in the pain pathway. Jpn J Pharmacol. 83(1):20-23.