Abstract
Histamine is a potent secretagogue for opioid pentapeptides (Met- and Leu-enkephalin) in adrenal chromaffin cells in vitro. This effect is dependent on extracellular Ca2+ and is reduced by Ca2+ channel blockers such as Co2+, 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-induced effects (acute release, changes in peptide cell content, proenkephalin A mRNA levels) are antagonized by the H1-receptor antagonist, clemastine, whereas the H2-receptor antagonists, ranitidine and cimetidine, were less effective (approximately 20% inhibition).
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adrenal Glands / drug effects
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Adrenal Glands / metabolism*
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Animals
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Calcium / physiology
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Cattle
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Cells, Cultured
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Chromaffin System / drug effects
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Chromaffin System / metabolism*
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Cimetidine / pharmacology
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Clemastine / pharmacology
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Cobalt / pharmacology
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Enkephalin, Leucine / biosynthesis*
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Enkephalin, Methionine / biosynthesis*
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Enkephalins / genetics
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Gallopamil / pharmacology
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Histamine / pharmacology*
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Histamine Antagonists / pharmacology
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Nifedipine / pharmacology
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Protein Precursors / genetics
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Pyrilamine / pharmacology
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RNA, Messenger / metabolism
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Ranitidine / pharmacology
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Receptors, Histamine / physiology*
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Receptors, Histamine H1 / physiology*
Substances
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Enkephalins
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Histamine Antagonists
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Protein Precursors
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RNA, Messenger
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Receptors, Histamine
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Receptors, Histamine H1
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proenkephalin
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Gallopamil
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Cobalt
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Enkephalin, Methionine
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Enkephalin, Leucine
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Cimetidine
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Histamine
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Ranitidine
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Clemastine
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cobaltous chloride
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Pyrilamine
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Nifedipine
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Calcium