β-Adrenergic agonists attenuate fibroblast-mediated contraction of released collagen gels

Tadashi Mio, Yuichi Adachi, Stefano Carnevali, Debra J. Romberger, John R. Spurzem, Stephen I. Rennard

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30 Scopus citations

Abstract

The effects of β-adrenergic agonists on fibroblast-mediated collagen gel contraction were investigated. β-Agonists isoproterenol and epinephrine significantly attenuated fibroblast-mediated gel contraction in a concentration-dependent manner, whereas α-agonist norepinephrine had no effect. The biologically active form of isoproterenol, (-)-isoproterenol, was 10-fold more effective than the optical isoform, (+)-isoproterenol. β- Antagonists sotalol and propranolol reversed the attenuation caused by 10- 7 M isoproterenol or epinephrine at the concentration of 10-7 M or 10-6 M, but the α-antagonist phentolamine did not. However, β1- or β2- specificity of these effects is not clear. Isobutyl methylxanthine augmented the effect of isoproterenol and also prolonged the duration. Two reagents which are known to increase intracellular adenosine 3',5'-cyclic monophosphate (cAMP), prostaglandin E2 and dibutyryl adenosine 3',5'-cyclic monophosphate, attenuated gel contraction in a concentration-dependent manner. These data suggest that the fibroblast-mediated collagen gel contraction can be modulated by β-adrenergic agonists and that the effect depends on cAMP.

Original languageEnglish (US)
Pages (from-to)L829-L835
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume270
Issue number5 14-5
StatePublished - May 1 1996

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Keywords

  • dibutyryl adenosine 3',5'-cyclic monophosphate
  • isoproterenol
  • salmeterol
  • terbutaline
  • wound retraction

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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