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Non‐adrenergic non‐cholinergic inhibition of gastrointestinal smooth muscle and its intracellular mechanism(s)
Author(s) -
Matsuda Nilce Mitiko,
Miller Steven M.
Publication year - 2010
Publication title -
fundamental and clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.655
H-Index - 73
eISSN - 1472-8206
pISSN - 0767-3981
DOI - 10.1111/j.1472-8206.2009.00761.x
Subject(s) - vasoactive intestinal peptide , chemistry , adenosine , cholinergic , intracellular , cyclic guanosine monophosphate , medicine , endocrinology , guanosine , nitric oxide , biochemistry , biology , receptor , neuropeptide
Relaxation of gastrointestinal smooth muscle caused by release of non‐adrenergic non‐cholinergic (NANC) transmitters from enteric nerves occurs in several physiologic digestive reflexes. Likely candidate NANC inhibitory agents include nitric oxide (NO), adenosine triphosphate (ATP), vasoactive intestinal peptide (VIP), pituitary adenylate cyclase‐activating peptide (PACAP), carbon monoxide (CO), protease‐activated receptors (PARs), hydrogen sulfide (H 2 S), neurotensin (NT) and beta‐nicotinamide adenine dinucleotide (β‐NAD). Multiple NANC transmitters work in concert, are pharmacologically coupled and are closely coordinated. Individual contribution varies regionally in the gastrointestinal tract and between species. NANC inhibition of gastrointestinal smooth muscle involves several intracellular mechanisms, including increase of cyclic guanosine monophosphate (cGMP), increase of cyclic adenosine monophosphate (cAMP) and hyperpolarization of the cell membrane via direct or indirect activation of potassium ion (K + ) channels.