CPI-17-deficient smooth muscle of chicken.

摘要: Ca2+ sensitivity of arterial contractility is governed by regulating myosin phosphatase activity in response to agonist stimuli. CPI-17, a inhibitor phosphoprotein, phosphorylated concomitantly with agonist-induced contractile sensitization mammalian artery. CPI-17 has not been detected chicken artery, but readily detectable pigeon To evaluate role we compared the arteries ‘CPI-17-deficient’ those CPI-17-rich rabbit and pigeon, studied effect CPI-17-reconstitution Other major regulatory/contractile proteins for are expressed both arteries. Agonists, such as an α1-agonist endothelin-1, produced significant contraction all species under physiological Ca2+-containing conditions. Depletion abolished these contractions partially inhibited them Unlike tissues, exerted little or endothelin-1. GTPγS slight sensitizing this was significantly smaller tissues. A PKC activator (PDBu) did generate rather reduced intact α-toxin-permeabilized artery contrast large Myosin light chain phosphorylation PDBu elevated Addition recombinant into β-escin-permeabilized restored PDBu-induced enhanced GTPγS-induced sensitization. Thus, essential G protein/PKC-mediated smooth muscle.