Purinergic mechanosensory transduction and visceral pain.
In this review, evidence is presented to support the hypothesis that mechanosensory transduction occurs in tubes and sacs and can initiate visceral pain. Experimental evidence for this mechanism in urinary bladder, ureter, gut, lung, uterus, tooth-pulp and tongue is reviewed. Potential therapeutic strategies are considered for the treatment of visceral pain in such conditions as renal colic, interstitial cystitis and inflammatory bowel disease by agents that interfere with mechanosensory transduction in the organs considered, including P2X3 and P2X2/3 receptor antagonists that are orally bioavailable and stable in vivo and agents that inhibit or enhance ATP release and breakdown.
Burnstock
Geoffrey
G
Autonomic Neuroscience Centre, Royal Free and University College Medical School, Rowland Hill Street, London NW3 2PF, UK. g.burnstock@ucl.ac.uk
D000818:Animals; D006801:Humans; D040542:Mechanotransduction, Cellular / Q000187:drug effects / Q000502:physiology*; D008954:Models, Biological; D010146:Pain / Q000378:metabolism / Q000503:physiopathology*; D058919:Purinergic P2 Receptor Antagonists; D058477:Receptors, Purinergic P2X3; D014781:Viscera / Q000294:innervation*
C546407:P2RX3 protein, human; D058919:Purinergic P2 Receptor Antagonists; D058477:Receptors, Purinergic P2X3