PKC regulates agonist-induced force enhancement in single α-toxin- permeabilized vascular smooth muscle cells

F. V. Brozovich

Research output: Contribution to journalArticle

18 Scopus citations

Abstract

To determine whether activation of protein kinase C (PKC) is involved in the mechanism of agonist-induced force enhancement, force and stiffness were measured in both Ca2+- and agonist-stimulated contractions of single isolated α-toxin-permeabilized smooth muscle cells. PKC function was inhibited with the pseudosubstrate inhibitor (residues 19-31) of PKC (PKI). For Ca2+ activation, PKI did not change (P > 0.05) steady-state force or stiffness. However, for agonist activation at pCa 7 (n = 13), PKI depressed force by 28.7 ± 4.5% (P < 0.05), in-phase stiffness by 35.4 ± 4.0% (P < 0.05), and quadrature stiffness by 25.6 ± 4.4% (P < 0.05), and for agonist activation at pCa 4 (n = 7), PKI depressed force by 25.8 ± 2.9% (P < 0.05), in-phase stiffness by 35.6 ± 5.6% (P < 0.05), and quadrature stiffness by 20.3 ± 4.1% (P < 0.05). These results suggest that the agonist-induced force enhancement in α-toxin-permeabilized smooth muscle is due to the activation of PKC.

Original languageEnglish (US)
Pages (from-to)C1202-C1206
JournalAmerican Journal of Physiology - Cell Physiology
Volume268
Issue number5 37-5
DOIs
StatePublished - 1995

Keywords

  • G proteins
  • latch
  • protein kinase C
  • pseudosubstrate inhibitory peptide
  • stiffness

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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