Protein kinase c regulates agonist induced force enhancement in single -
toxin permeabilized vascular smooth muscle cells.
Brozovich, Frank V.
Division of Cardiology, 2074 Abington Road, Cleveland, OH
44106-5038, (216)368-1643, FAX(216)368-5586, E-mail: fxb9@po.cwru.edu
APStracts 2:0038C, 1995.
To determine if 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
-toxin permeabilized smooth muscle cells. PKC function was inhibited with the
pseudosubstrate inhibitor (PKI) of PKC (residues 19-31). 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 -toxin permeabilized
smooth muscle is due to the activation of protein kinase C.
Received 5 August 1994; accepted in final form 21 November 1994
APS Manuscript Number C0463-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1994 The American Physiological Society.
Published in APStracts on 27 February 1995.