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pubmed:abstractText |
This study examined the mechanism of action of neurotensin on intraluminal pressure in rat proximal colon. The direct and indirect contractile response to neurotensin (100 nM) was abolished in Ca(2+)-free solution, and was antagonized by nifedipine (1-5-10 nM) and potentiated by Bay K 8644 (methyl 1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl)- pyridine-5-carboxylate) (10-100-1000 nM). Neurotensin, in the presence of nifedipine (10 nM) and atropine (1 microM), induced a tetrodotoxin-insensitive inhibitory effect, which was antagonized by SR 48692 (2[(1-(7-chloro-4-quinolinyl)-5-(2,6-dimethoxy-phenyl)pyrazol-3-yl) carbonyl amino]tricyclo (3.3.1.1.(3.7)) decan-2-carboxylic acid) (300 nM) or apamin (0.1 microM). The results demonstrate that the neurotensin response is dependent on the influx of Ca2+ via L-type channels and results from summation of excitatory and inhibitory effects.
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