Role of protein kinase C in calcium sensitization during muscarinic stimulation in airway smooth muscle

Dorothee H. Bremerich, David O. Warner, Robert R. Lorenz, Robin Shumway, Keith A. Jones

Research output: Contribution to journalArticlepeer-review

44 Scopus citations


Muscarinie receptor stimulation increases Ca2+ sensitivity, i.e., the amount of force produced at a constant submaximal cytosolic Ca2+ concentration ([Ca2+](i)), in permeabilized smooth muscle preparations. It is controversial whether this increase in Ca2+ sensitivity is in part mediated by protein kinase C (PKC). With the use of a β-escin permeabilized canine tracheal smooth muscle (CTSM) preparation, the effect of four putative PKC inhibitors [calphostin C, chelerythrine chloride, a pseudosubstrate inhibitor for PKC [PKC peptide-(19-31)], and staurosporine) on Ca2+ sensitization induced by acetylcholine (ACh) plus GTP was determined. Proincubation with each of the inhibitors did not effect subsequent Ca2+ sensitization induced by muscarinic receptor stimulation in the presence of a constant submaximal [Ca2+](i), neither did any of these compounds reverse the increase in Ca2+ sensitivity induced by ACh plus GTP. Administration of a 1,2-diacylglycerol analog, 1-oleoyl-2-acetyl-sn-glycerol, did not induce Ca2+ sensitization at a constant submaximal [Ca2+](i). Thus we found no evidence that PKC mediates increases in Ca2+ sensitivity produced by muscarinic receptor stimulation in permeabilized CTSM.

Original languageEnglish (US)
Pages (from-to)L775-L781
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number4 17-4
StatePublished - 1997


  • Activator
  • Calcium sensitivity
  • Canine
  • Lung
  • Protein kinase C inhibitors
  • Second messenger systems
  • Trachea
  • β-escin

ASJC Scopus subject areas

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


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