Involvement of vasoactive intestinal polypeptide in nicotine‐induced relaxation of the rat gastric fundus

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Abstract
Nicotine‐induced relaxation and release of vasoactive intestinal polypeptide (VIP)‐ and peptide histidine isoleucine (PHI)‐like immunoreactivity (LI) were measured in longitudinal muscle strips from the rat gastric fundus. Under non‐cholinergic conditions (0.3μm atropine), nicotine (3–300 μm) produced concentration‐dependent relaxations of the 5‐hydroxytryptamine (3μm)‐precontracted strips. Under non‐adrenergic non‐cholinergic (NANC) conditions (0.3μm atropine+1μm phentolamine+1μm nadolol), relaxations induced by sub‐maximal nicotine concentrations (10 and 30μm) were significantly smaller, while that produced by the highest concentration used (300μm) was similar to that seen under non‐cholinergic conditions. Re‐exposure to the same nicotine concentration 1h later induced smaller relaxations, indicating desensitization. The reductions seen in the second responses were proportional to the concentration used. Under non‐cholinergic conditions, the relaxant response to 30μm nicotine was abolished by hexamethonium (100μm) and significantly reduced by tetrodotoxin (TTX, 3μm). The TTX‐resistant component was not observed under NANC conditions. NANC relaxation induced by 30μm nicotine was significantly reduced by a specific anti‐VIP serum (approximately 35% less than that seen with normal rabbit serum). Nicotine (30–300μm) caused significant, concentration‐dependent increases in the outflow of VIP‐ and PHI‐LI from the strips; these effects were also diminished with re‐exposure. The increases in both types of immunoreactivity evoked by nicotine (300μm) were abolished by hexamethonium (300μm), TTX (3μm) and a calcium‐free medium. These findings indicate that VIP and possibly PHI are involved in NANC relaxation of the rat gastric fundus induced by nicotine.

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