6533b858fe1ef96bd12b5ab9

RESEARCH PRODUCT

STIMULATION OF ?1-ADRENOCEPTORS ENHANCES ELECTRICALLY EVOKED [3H]-ACETYLCHOLINE RELEASE FROM RAT PHRENIC NERVE

I. WesslerG. HolzerA. Künster

subject

MaleAgonistmedicine.medical_specialtyPhysiologymedicine.drug_classAdrenergic beta-AntagonistsNeuromuscular transmissionStimulationPropranololIn Vitro TechniquesTritiumNorepinephrinePhentolaminePhysiology (medical)IsoprenalineInternal medicineReceptors Adrenergic betamedicineAnimalsPhentolamineFenoterolFenoterolPharmacologyChemistryImidazolesIsoproterenolRats Inbred StrainsPropranololAcetylcholineElectric StimulationRatsPhrenic NerveEndocrinologyFemaleAcetylcholinemedicine.drug

description

1. The effects of isoprenaline, noradrenaline and fenoterol on the electrically evoked release of [3H]-acetylcholine from the rat phrenic nerve were investigated. 2. Isoprenaline (0.1 mumol/L) and noradrenaline (1 mumol/L) enhanced evoked [3H]-acetylcholine release by about 90%, an effect which was abolished by CGP 20712A (0.1 mumol/L), a specific antagonist at beta 1-adrenoceptors. Noradrenaline still enhanced [3H]-acetylcholine release in the presence of phentolamine (1 mumol/L). 3. The enhancing effect of both isoprenaline and noradrenaline decreased at prolonged exposure times (24-32 min). A pre-exposure of the tissue to a low concentration (0.01 mumol/L) of isoprenaline prevented the enhancing effect of 0.1 mumol/L isoprenaline. 4. Fenoterol, a specific agonist at beta 2-adrenoceptors, did not modify evoked [3H]-acetylcholine release. 5. The present results indicate the existence of facilitatory beta 1-adrenoceptors on the motor nerve. These receptors appear to be desensitized either by a high concentration of, or by a long exposure to, agonists. Under the present conditions noradrenaline enhances the release of newly synthesized transmitter mainly by stimulation of beta-adrenoceptors.

https://doi.org/10.1111/j.1440-1681.1990.tb01261.x