It is well known that the regulation of contractile mechanisms of intestinal smooth muscle involves neural control mechanisms through extrinsic (sympathetic and parasympathetic) and intrinsic (myenteric and submucosal plexus) pathways in addition to myogenic contractions
. The major regulatory mechanisms of intestinal smooth muscle contractility involve cholinergic, adrenergic, and nonadrenergic-noncholinergic systems.
These results indicated that taurine might exert dual modulation not on myogenic contractions
of intestinal smooth muscle directly, but by some other mechanisms, e.g., regulation of neurotransmitter or hormone release.
While no single set of data or hypothesis explains all involuntary contractions or occurrences of urgency/frequency, four concepts seem to be valid: 1) patients with OAB have faulty central inhibition, which leads to enhancement of excitatory neurotransmission in the micturition reflex pathway (neurogenic); 2) there is partial denervation of smooth muscle, which leads to co-ordinated myogenic contractions
and increased bladder pressure (myogenic); 3) there is a "leaking" of acetylcholine from parasympathetic nerves during filling/storage, which leads to afferent activation (neurogenic-myogenic); and 4) abnormal signals originating in the urothelium are influenced by generation and release of local mediators (e.g., acetylcholine, nitric oxide, urothelial-derived inhibitory factor).