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

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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 Ca(2+)- and agonist-stimulated contractions of single isolated alpha-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 alpha-toxin-permeabilized smooth muscle is due to the activation of PKC.