Histamine acting on a histamine type 1 (H1) receptor increases beta-glucuronidase release from human lung macrophages.

M. Cluzel, M. C. Liu, D. W. Goldman, B. J. Undem, L. M. Lichtenstein

Research output: Contribution to journalArticle

Abstract

The effects of histamine on lung macrophages have been studied by both biologic and radioligand experiments. After overnight adherence, lung macrophages spontaneously released beta-glucuronidase (beta-G) at a rate of approximately 7 nmol of hydrolyzed substrate/h/million cells. Histamine at low concentrations (10(-9) to 10(-8) M) resulted in a consistent potentiation of this release. The concentration-effect curve of histamine was bell-shaped, reaching an optimum at 10(-9) M, with concentrations greater than 10(-8) M having no significant effect. At a maximally effective concentration (10(-9) M), histamine evoked a 135 +/- 9.6% (mean +/- SE; n = 8, P less than 0.001) potentiation in the total amount of beta-G released during the first 60 min of incubation. This increase in beta-G release represented both a slight increase in beta-G synthesis as well as an increase in the percentage of beta-G released. When the secreted beta-G is expressed as a percentage of total content, histamine (10(-9) M) evoked a 125 +/- 3.2% (mean +/- SE; n = 27, P less than 0.0005) enhancement. The potentiation of beta-G release by histamine was evident after 45 min of incubation and persisted for up to 6 h. The potentiation of beta-G by histamine was sensitive to inhibition by pyrilamine (10(-7) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Original languageEnglish (US)
Pages (from-to)603-609
Number of pages7
JournalAmerican journal of respiratory cell and molecular biology
Volume3
Issue number6
DOIs
StatePublished - Dec 1990

ASJC Scopus subject areas

  • Molecular Biology
  • Pulmonary and Respiratory Medicine
  • Clinical Biochemistry
  • Cell Biology

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