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Urothelium‐derived inhibitory factor(s) influences on detrusor muscle contractility in vitro
Author(s) -
Hawthorn M H,
Chapple C R,
Cock M,
ChessWilliams R
Publication year - 2000
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0703068
Subject(s) - urothelium , carbachol , detrusor muscle , endocrinology , muscarinic acetylcholine receptor , purinergic receptor , apamin , chemistry , medicine , inhibitory postsynaptic potential , electrical impedance myography , urinary bladder , adenosine , stimulation , biology , vasodilation , receptor , potassium channel
The function of the bladder urothelium in modulating contractile responses of the underlying detrusor smooth muscle to muscarinic stimulation has been examined in the pig bladder. Saturation curves for [ 3 H]‐QNB binding demonstrated a greater muscarinic receptor density in the urothelium than in the detrusor smooth muscle. The presence of an intact urothelium on isolated bladder strips inhibited contractions induced by carbachol but not KCl. Contractions of a urothelium‐denuded muscle strip were inhibited in the presence of a second bladder strip with an intact urothelium, but not if the second strip was denuded. The urothelium‐induced inhibition of contractions was not prevented in the presence of L ‐NOARG, methylene blue, indomethacin, propranolol, suramin, TEA or apamin. The data suggest the presence of a diffusable, urothelium‐derived inhibitory factor, which could not be identified but appears to be neither nitric oxide, a cyclo‐oxygenase product, a catecholamine, adenosine, GABA nor an EDHF sensitive to apamin. British Journal of Pharmacology (2000) 129 , 416–419; doi: 10.1038/sj.bjp.0703068