6533b838fe1ef96bd12a4775
RESEARCH PRODUCT
Calcium dependence of the contraction produced by endothelin (ET-1) in isolated guinea-pig trachea.
Charles AdvenierEsteban J. MorcilloBenjamín SarriáJulio CortijoJuan V. EspluguesEmmanuel Nalinesubject
Malemedicine.medical_specialtyContraction (grammar)NicardipineGuinea PigsIndomethacinchemistry.chemical_elementCalciumBiologyIn Vitro TechniquesPotassium ChlorideGuinea pigInternal medicinemedicineExtracellularAnimalsDiltiazemPharmacologyEndothelinsMuscle Smooth3-Pyridinecarboxylic acid 14-dihydro-26-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl esterCalcium Channel BlockersTracheaEndocrinologychemistryVerapamilCalciumEndothelin receptormedicine.drugMuscle Contractiondescription
Endothelin (ET-1, 1 pM to 0.1 microM) produced a concentration-dependent contraction of isolated guinea-pig trachea. BAY K 8644 (1 microM) did not significantly alter the concentration-response curve for ET-1. Incubation with nicardipine (10 microM) partly inhibited responses to low concentrations (10 pM to 1 nM) of ET-1 while verapamil (10 microM) and diltiazem (10 microM) were ineffective. La3+ (10 microM) and Cd2+ (10 microM) preferentially depressed the responses evoked by high concentrations (30 nM-0.1 microM) of ET-1 without affecting the responses evoked by low concentrations of the peptide. Incubation in Ca2(+)-free (with EDTA, 1 mM) medium resulted in suppression of the responses elicited by low concentrations of ET-1 and partial inhibition of the responses elicited by high concentrations of the peptide. It is concluded that responses to ET-1 are dependent on extracellular Ca2+. The promotion of Ca2+ entry by ET-1 is not confined to a particular class of Ca2+ channel. An intracellular source of Ca2+ is also mobilized by high concentrations (greater than 10(-9) M) of ET-1.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1990-10-01 | European journal of pharmacology |