TY - JOUR
T1 - Stimulation by nicotine of enteric inhibitory nerves and release of vasoactive intestinal peptide in the taenia of the guinea-pig caecum
AU - Iselin, Christophe E.
AU - Martin, Jean Luc
AU - Magistretti, Pierre J.
AU - Ferrero, Jean D.
PY - 1988/3/29
Y1 - 1988/3/29
N2 - The stimulation by nicotine of intramural nerves and the role of ATP and vasoactive intestinal peptide (VIP) as inhibitory transmitters were studied in the isolated taenia of the guinea-pig caecum. Nicotine (4-32 μM) caused transient, concentration-dependent relaxations which were unaffected by atropine, prazosin or sotalol. Drugs with membrane-stabilizing activity, such as dl-propranolol (0.5 μM), d-propranolol (0.5 μM) or lidocaine (10 μM) antagonized the nicotine-induced relaxation without modifying the response to electrical field stimulation. Similar results were obtained with the cyclooxygenase inhibitor, indomethacin (2.8 μM). Nucleotide pyrophosphatase (0.5 (U/ml), which hydrolyzes ATP to AMP, reversibly inhibited the response to nicotine but the response to field stimulation was not decreased. Nicotine evoked a calcium-dependent release of VIP, which was blocked by tetrodotoxin (1 μM), d-propranolol (0.5 μM) or, as previously shown, by apamin (0.2 μM). The finding that nicotine-induced relaxation was accompanied by the neuronal release of VIP is compatible with the possibility that VIP is an inhibitory transmitter but is not definitive evidence, since it could have been due to the stimulation of distinct populations of nerves by nicotine.
AB - The stimulation by nicotine of intramural nerves and the role of ATP and vasoactive intestinal peptide (VIP) as inhibitory transmitters were studied in the isolated taenia of the guinea-pig caecum. Nicotine (4-32 μM) caused transient, concentration-dependent relaxations which were unaffected by atropine, prazosin or sotalol. Drugs with membrane-stabilizing activity, such as dl-propranolol (0.5 μM), d-propranolol (0.5 μM) or lidocaine (10 μM) antagonized the nicotine-induced relaxation without modifying the response to electrical field stimulation. Similar results were obtained with the cyclooxygenase inhibitor, indomethacin (2.8 μM). Nucleotide pyrophosphatase (0.5 (U/ml), which hydrolyzes ATP to AMP, reversibly inhibited the response to nicotine but the response to field stimulation was not decreased. Nicotine evoked a calcium-dependent release of VIP, which was blocked by tetrodotoxin (1 μM), d-propranolol (0.5 μM) or, as previously shown, by apamin (0.2 μM). The finding that nicotine-induced relaxation was accompanied by the neuronal release of VIP is compatible with the possibility that VIP is an inhibitory transmitter but is not definitive evidence, since it could have been due to the stimulation of distinct populations of nerves by nicotine.
KW - ATP
KW - Enteric inhibitory nerves
KW - Nicotine
KW - Taenia caeci
KW - Vasoactive intestinal peptide (VIP)
UR - http://www.scopus.com/inward/record.url?scp=0023906192&partnerID=8YFLogxK
U2 - 10.1016/0014-2999(88)90562-6
DO - 10.1016/0014-2999(88)90562-6
M3 - Article
C2 - 2837398
AN - SCOPUS:0023906192
SN - 0014-2999
VL - 148
SP - 179
EP - 186
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 2
ER -