Calcium sensitization produced by G protein activation in airway smooth muscle.

Academic Article

Abstract

  • We determined whether activation of G proteins can affect the force developed for a given intracellular Ca(2+) concentration ([Ca(2+)]; i.e., the Ca(2+) sensitivity) by mechanisms in addition to changes in regulatory myosin light chain (rMLC) phosphorylation. Responses in alpha-toxin-permeabilized canine tracheal smooth muscle were determined with Ca(2+) alone or in the presence of ACh, endothelin-1 (ET-1), or aluminum fluoride (AlF; acute or 1-h exposure). Acute exposure to each compound increased Ca(2+) sensitivity without changing the response to high [Ca(2+)] (maximal force). However, chronic exposure to AlF, 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 AlF exposure required Ca(2+) 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 Ca(2+) sensitivity in airways by additional mechanisms that are independent of rMLC phosphorylation.
  • Authors

    Keywords

  • Acetylcholine, Adenosine Triphosphate, Aluminum Compounds, Animals, Calcium, Dogs, Drug Resistance, Endothelin-1, Female, Fluorides, GTP-Binding Proteins, In Vitro Techniques, Magnesium Compounds, Male, Muscle Contraction, Muscle, Smooth, Myosin Light Chains, Phosphorylation, Time Factors, Trachea
  • Digital Object Identifier (doi)

    Author List

  • Yoshimura H; Jones KA; Perkins WJ; Kai T; Warner DO
  • Start Page

  • L631
  • End Page

  • L638
  • Volume

  • 281
  • Issue

  • 3