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1 Boston Biomedical Research Institute, 64 Grove Street, Watertown, MA 02472, USA2 Center for Cell Signalling, University of Virginia, 1400 Jefferson Park Avenue, Charlottesville, VA 22908, USA
Ca2+ sensitivity of arterial contractility is governed by regulating myosin phosphatase activity in response to agonist stimuli. CPI-17, a myosin phosphatase inhibitor phosphoprotein, is phosphorylated concomitantly with agonist-induced contractile Ca2+ sensitization in mammalian artery. CPI-17 has not been detected in chicken artery, but is readily detectable in pigeon artery. To evaluate a role of CPI-17, we compared contractility of the arteries of ‘CPI-17-deficient’ chicken with those of CPI-17-rich rabbit and pigeon, and studied the effect of CPI-17-reconstitution in chicken artery. Other major regulatory/contractile proteins for Ca2+ sensitization are expressed in both chicken and rabbit arteries. Agonists, such as an 
1-agonist and endothelin-1, produced significant contraction in arteries of all species under physiological Ca2+-containing conditions. Depletion of Ca2+ abolished these contractions in chicken but partially inhibited them in rabbit and pigeon arteries. Unlike CPI-17-rich tissues, chicken arteries exerted little Ca2+ sensitization in response to 1-agonist or endothelin-1. GTP
S produced a slight Ca2+ sensitizing effect in chicken artery, but this was significantly smaller compared with CPI-17-rich tissues. A PKC activator (PDBu) did not generate but rather reduced a contraction in both intact and -toxin-permeabilized chicken artery in contrast to a large contraction in CPI-17-rich arteries. Myosin light chain phosphorylation was reduced by PDBu in chicken but elevated in rabbit artery. Addition of recombinant CPI-17 into ß-escin-permeabilized chicken artery restored PDBu-induced and enhanced GTPS-induced Ca2+ sensitization. Thus, CPI-17 is essential for G protein/PKC-mediated Ca2+ sensitization in smooth muscle.
(Received 15 March 2004;
accepted after revision 16 April 2004;
first published online 16 April 2004)
Corresponding author T. Kitazawa: Boston Biomedical Research Institute, 64 Grove Street, Watertown, MA 02472, USA. Email: kitazawa{at}bbri.org
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