作者: Hideo Kanaide
DOI: 10.1007/978-1-4613-1235-2_23
关键词: Contractility 、 Stimulation 、 Depolarization 、 Myosin light-chain kinase 、 Kinase 、 Chemistry 、 Phosphorylation 、 Biophysics 、 Vascular smooth muscle 、 Contraction (grammar)
摘要: The contraction of vascular smooth muscle is regulated mainly by changes in the cytosolic calcium concentration ([Ca2+]i), and thus development force has been regarded as a good indicator an increase [Ca2+]i [1]. initiated subsequent phosphorylation myosin light chain complex Ca2+-calmodulin kinase [2]. It demonstrated that, for given elevation [Ca2+]i, receptor-mediated stimulation various agonists caused proportionally greater than did depolarization with high K+ solutions [3–8]. While it generally accepted that depends on Ca2+-mediated phosphorylation, could be maintained under lower levels through other Ca2+-insensitive mechanisms such latch bridges [9] or cooperating cycling cross-bridges [10]. Using receptor-coupled per-meabilized staphylococcal α-toxin [11] β-escin [12], was Ca2+ sensitivity contractile apparatus modulated receptor-G-protein-coupled mechanism. A protein C-mediated mechanism proposed to explain agonist-modulated contractility [6–8].