Calcium sensitization produced by G protein activation in airway smooth muscle

Hayashi Yoshimura, Keith A. Jones, William J. Perkins, Kai Tetsuya, David O. Warner

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

We determined whether activation of G proteins can affect the force developed for a given intracellular Ca2+ concentration ([Ca2+]; i.e., the Ca2+ sensitivity) by mechanisms in addition to changes in regulatory myosin light chain (rMLC) phosphorylation. Responses in α-toxin-permeabilized canine tracheal smooth muscle were determined with Ca2+ alone or in the presence of ACh, endothelin-1 (ET-1), or aluminum fluoride (AlF4- acute or 1-h exposure). Acute exposure to each compound increased Ca2+ sensitivity without changing the response to high [Ca2+] (maximal force). However, chronic exposure to AlF4-, but not to chronic ACh or ET-1, increased maximal force by increasing the force produced for a given rMLC phosphorylation. Studies employing thiophosphorylation of rMLC showed that the increase in force produced by chronic AlF4- exposure required Ca2+ during activation to be manifest. Unlike the acute response to receptor agonists, which is mediated solely by increases in rMLC phosphorylation, chronic direct activation of G proteins further increases Ca2+ sensitivity in airways by additional mechanisms that are independent of rMLC phosphorylation.

Original languageEnglish (US)
Pages (from-to)L631-L638
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume281
Issue number3 25-3
DOIs
StatePublished - 2001

Keywords

  • Airway inflammation
  • Aluminum fluoride
  • Regulatory myosin light chain phosphorylation
  • Remodeling

ASJC Scopus subject areas

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

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