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Histamine Affects Release and Biosynthesis of Opioid Peptides Primarily via H 1 ‐Receptors in Bovine Chromaffin Cells
Author(s) -
Bommer Michael,
Liebisch Daniel,
Kley Nikolai,
Herz Albert,
Noble Ernest
Publication year - 1987
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1987.tb02426.x
Subject(s) - histamine , proenkephalin , secretagogue , cimetidine , opioid peptide , receptor , medicine , chemistry , endocrinology , enkephalin , extracellular , chromaffin cell , histamine h2 receptor , antagonist , opioid , biology , biochemistry , adrenal medulla , catecholamine
Histamine is a potent secretagogue for opioid pentapeptides (Met‐ and Leu‐enkephalin) in adrenal chromaffin cells in vitro. This effect is dependent on extracellular Ca 2+ and is reduced by Ca 2+ channel blockers such as Co 2+ , D 600, and nifedipine. Moreover, histamine also produced a profound compensatory increase in cellular peptide content after 48 h of exposure, most likely caused by a four‐ to fivefold increase in the mRNA levels coding for the proenkephalin A precursor. All the histamine‐in‐duced effects (acute release, changes in peptide cell content, proenkephalin A mRNA levels) are antagonized by the H 1‐ receptor antagonist, clemastine, whereas the H 2 ‐receptor antagonists, ranitidine and cimetidine, were less effective (∼20% inhibition).