6533b82ffe1ef96bd1295315
RESEARCH PRODUCT
Mode and mechanism of neurotensin action in rat proximal colon
Rosa SerioFlavia Mulèsubject
Atropinemedicine.medical_specialtyNifedipineColonchemistry.chemical_elementCholinergic AgonistsIn Vitro TechniquesCalciumInhibitory postsynaptic potentialApaminCholinergic Antagonistschemistry.chemical_compoundNifedipineInternal medicinemedicineAnimalsReceptors NeurotensinRats WistarNeurotensinPharmacologyChemistryMuscle Smooth3-Pyridinecarboxylic acid 14-dihydro-26-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl esterBethanecholCalcium Channel BlockersRatsCalcium Channel AgonistsEndocrinologyApaminMechanism of actionQuinolinesExcitatory postsynaptic potentialBiophysicsPyrazolesCalciummedicine.symptomMuscle Contractionmedicine.drugMuscle contractionNeurotensindescription
Abstract 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 μM), 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 μM). The results demonstrate that the neurotensin response is dependent on the influx of Ca 2+ via L-type channels and results from summation of excitatory and inhibitory effects.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1997-01-29 | European Journal of Pharmacology |