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Involvement of vasoactive intestinal polypeptide in nicotine-induced relaxation of the rat gastric fundus.
Br J Pharmacol. 1997 Jul; 121(6):1105-12.BJ

Abstract

1. 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. 2. Under non-cholinergic conditions (0.3 microM atropine), nicotine (3-300 microM) produced concentration-dependent relaxations of the 5-hydroxytryptamine (3 microM)-precontracted strips. Under non-adrenergic non-cholinergic (NANC) conditions (0.3 microM atropine + 1 microM phentolamine + 1 microM nadolol), relaxations induced by sub-maximal nicotine concentrations (10 and 30 microM) were significantly smaller, while that produced by the highest concentration used (300 microM) was similar to that seen under non-cholinergic conditions. 3. Re-exposure to the same nicotine concentration 1 h later induced smaller relaxations, indicating desensitization. The reductions seen in the second responses were proportional to the concentration used. 4. Under non-cholinergic conditions, the relaxant response to 30 microM nicotine was abolished by hexamethonium (100 microM) and significantly reduced by tetrodotoxin (TTX, 3 microM). The TTX-resistant component was not observed under NANC conditions. 5. NANC relaxation induced by 30 microM nicotine was significantly reduced by a specific anti-VIP serum (approximately 35% less than that seen with normal rabbit serum). 6. Nicotine (30-300 microM) 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 (300 microM) were abolished by hexamethonium (300 microM), TTX (3 microM) and a calcium-free medium. 7. These findings indicate that VIP and possibly PHI are involved in NANC relaxation of the rat gastric fundus induced by nicotine.

Authors+Show Affiliations

Institute of Pharmacology, Catholic University School of Medicine, Rome, Italy.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9249245

Citation

Curro, D, and P Preziosi. "Involvement of Vasoactive Intestinal Polypeptide in Nicotine-induced Relaxation of the Rat Gastric Fundus." British Journal of Pharmacology, vol. 121, no. 6, 1997, pp. 1105-12.
Curro D, Preziosi P. Involvement of vasoactive intestinal polypeptide in nicotine-induced relaxation of the rat gastric fundus. Br J Pharmacol. 1997;121(6):1105-12.
Curro, D., & Preziosi, P. (1997). Involvement of vasoactive intestinal polypeptide in nicotine-induced relaxation of the rat gastric fundus. British Journal of Pharmacology, 121(6), 1105-12.
Curro D, Preziosi P. Involvement of Vasoactive Intestinal Polypeptide in Nicotine-induced Relaxation of the Rat Gastric Fundus. Br J Pharmacol. 1997;121(6):1105-12. PubMed PMID: 9249245.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of vasoactive intestinal polypeptide in nicotine-induced relaxation of the rat gastric fundus. AU - Curro,D, AU - Preziosi,P, PY - 1997/7/1/pubmed PY - 1997/7/1/medline PY - 1997/7/1/entrez SP - 1105 EP - 12 JF - British journal of pharmacology JO - Br. J. Pharmacol. VL - 121 IS - 6 N2 - 1. 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. 2. Under non-cholinergic conditions (0.3 microM atropine), nicotine (3-300 microM) produced concentration-dependent relaxations of the 5-hydroxytryptamine (3 microM)-precontracted strips. Under non-adrenergic non-cholinergic (NANC) conditions (0.3 microM atropine + 1 microM phentolamine + 1 microM nadolol), relaxations induced by sub-maximal nicotine concentrations (10 and 30 microM) were significantly smaller, while that produced by the highest concentration used (300 microM) was similar to that seen under non-cholinergic conditions. 3. Re-exposure to the same nicotine concentration 1 h later induced smaller relaxations, indicating desensitization. The reductions seen in the second responses were proportional to the concentration used. 4. Under non-cholinergic conditions, the relaxant response to 30 microM nicotine was abolished by hexamethonium (100 microM) and significantly reduced by tetrodotoxin (TTX, 3 microM). The TTX-resistant component was not observed under NANC conditions. 5. NANC relaxation induced by 30 microM nicotine was significantly reduced by a specific anti-VIP serum (approximately 35% less than that seen with normal rabbit serum). 6. Nicotine (30-300 microM) 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 (300 microM) were abolished by hexamethonium (300 microM), TTX (3 microM) and a calcium-free medium. 7. These findings indicate that VIP and possibly PHI are involved in NANC relaxation of the rat gastric fundus induced by nicotine. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/9249245/Involvement_of_vasoactive_intestinal_polypeptide_in_nicotine_induced_relaxation_of_the_rat_gastric_fundus_ L2 - https://doi.org/10.1038/sj.bjp.0701245 DB - PRIME DP - Unbound Medicine ER -