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MODIFICATION OF ENDORPHIN/ENKEPHALIN ANALGESIA AND STRESS‐INDUCED ANALGESIA BY DIVALENT CATIONS, A CATION CHELATOR AND AN IONOPHORE
Author(s) -
CHAPMAN D.B.,
WAY E. LEONG
Publication year - 1982
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1982.tb08799.x
Subject(s) - chemistry , divalent , enkephalin , (+) naloxone , ionophore , chelation , pharmacology , nociception , calcium , medicine , biochemistry , antagonist , opioid , receptor , inorganic chemistry , organic chemistry
1 The possibility that divalent cations may antagonize opiate peptide analgesia and stress‐induced analgesia was examined. 2 Intracerebroventricular injection of low doses of Ca 2+ , Mn 2+ and Mg 2+ antagonized β‐endorphin and methionine‐enkephalin analgesia. Ba 2+ and Cd 2+ were without effect. 3 The ionophore, A23187, significantly antagonized β‐endorphin analgesia and the effect was increased when a low dose of Ca 2+ was injected at the same time as the ionophore. 4 Ethylene glycol tetraacetic acid (but not ethylenediamine tetraacetic acid) significantly potentiated endorphin analgesia. 5 Stress‐induced analgesia, as determined by increased tail‐flick latencies following intraperitoneal injection of acetic acid, was effectively antagonized by naloxone, Ca 2+ and Mn 2+ . The frequency of writhing following acetic acid injection was increased by both naloxone and divalent metal ions, again suggesting antagonism of endogenous opiates. 6 These results confirm previous findings indicating that divalent metal ions (and especially Ca 2+ ) may be involved in the actions of opiates.