Histamine affects release and biosynthesis of opioid peptides primarily via H1-receptors in bovine chromaffin cells.

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).