Regulation of the Ca(2+)-force relationship in permeabilized arterial smooth muscle.

摘要: It is generally accepted that the primary trigger for smooth muscle contraction elevation of intracellular Ca2+ concentration ([Ca2+]i) and subsequent phosphorylation myosin light chain (MLC) by Ca2+-calmodulin dependent MLC kinase (for reviews see Kamm Stull, 1985; Somlyo, 1985). However, simultaneous measurements tension [Ca2+]i in intact tissues have shown during continuous stimulation, although a-adrenergic agonist induced force maintained at high constant levels, falls close to basal concentrations (Morgan Morgan, 1982; 1984a). has also been demonstrated levels both shortening velocity fall suprabasal phase maintenance (Dillon et al., 1981). In order account these phenomena, a sensitivity state, latch was proposed be important developed face significant decreases Similar increases Ca2+-force relationship, skinned preparations addition exogenous calmodulin (Cassidy 1981; Ruegg Paul, 1982), an initial stimulation [Ca2+] followed exposure lower (Chatterjee Murphy, Moreland 1986), phorbol esters Tajeda, 1986; Itoh 1988) or GTPγS (Fujiwara 1989). until recently it not possible increase physiological mode stimulation. Recent studies utilizing Staphylcoccal α-toxin permeabilized preparation receptor plus GTP can produce level additional force, fixed submaximal [Ca2+], as compared response alone (Nishimura 1988; Kitazawa 1989; Kobavashi