Combettes L, Berthon B, Binet A, Claret M
Biochem J. 1986 Aug 1;237(3):675-83. doi: 10.1042/bj2370675.
The effects of glucagon and vasopressin, singly or together, on cytosolic free Ca2+ concentration [( Ca2+]i) and on the 45Ca2+ efflux were studied in isolated rat liver cells. In the presence of 1 mM external Ca2+, glucagon and vasopressin added singly induced sustained increases in [Ca2+]i. The rate of the initial fast phase of the [Ca2+]i increase and the magnitude of the final plateau were dependent on the concentrations (50 pm-0.1 microM) of glucagon and vasopressin. Preincubating the cells with a low concentration of glucagon (0.1 nM) for 2 min markedly accelerated the fast phase and elevated the plateau of the [Ca2+]i increase caused by vasopressin. In the absence of external free Ca2+, glucagon and vasopressin transiently increased [Ca2+]i and stimulated the 45Ca2+ efflux from the cells, indicating mobilization of Ca2+ from internal store(s). Preincubating the cells with 0.1 nM-glucagon accelerated the rate of the fast phase of the [Ca2+]i rise caused by the subsequent addition of vasopressin. However, unlike what was observed in the presence of 1 mM-Ca2+, glucagon no longer enhanced the maximal [Ca2+]i response to vasopressin. In the absence of external free Ca2+, higher concentrations (1 nM-0.1 microM) of glucagon, which initiated larger increases in [Ca2+]i, drastically decreased the subsequent Ca2+ response to vasopressin (10 nM). At these concentrations, glucagon also decreased the vasopressin-stimulated 45Ca2+ efflux from the cells. It is suggested that, in the liver, glucagon accelerates the fast phase and elevates the plateau of the vasopressin-mediated [Ca2+]i increase respectively by releasing Ca2+ from the same internal store as that permeabilized by vasopressin, probably the endoplasmic reticulum, and potentiating the influx of extracellular Ca2+ caused by this hormone.
研究了胰高血糖素和血管加压素单独或共同作用对离体大鼠肝细胞胞质游离钙离子浓度[Ca2+]i以及45Ca2+外流的影响。在存在1 mM细胞外钙离子的情况下,单独添加胰高血糖素和血管加压素均可诱导[Ca2+]i持续升高。[Ca2+]i升高的初始快速相速率和最终平台期幅度取决于胰高血糖素和血管加压素的浓度(50皮摩尔-0.1微摩尔)。用低浓度胰高血糖素(0.1纳摩尔)预孵育细胞2分钟可显著加速快速相,并提高血管加压素引起的[Ca2+]i升高的平台期。在不存在细胞外游离钙离子的情况下,胰高血糖素和血管加压素可短暂升高[Ca2+]i,并刺激细胞内45Ca2+外流,表明钙离子从内部储存库中动员出来。用0.1纳摩尔胰高血糖素预孵育细胞可加速随后添加血管加压素引起的[Ca2+]i升高的快速相速率。然而,与在1 mM钙离子存在下观察到的情况不同,胰高血糖素不再增强对血管加压素的最大[Ca2+]i反应。在不存在细胞外游离钙离子的情况下,较高浓度(1纳摩尔-0.1微摩尔)的胰高血糖素可引发更大的[Ca2+]i升高,从而显著降低随后对血管加压素(10纳摩尔)的钙离子反应。在这些浓度下,胰高血糖素还可降低血管加压素刺激的细胞内45Ca2+外流。提示在肝脏中,胰高血糖素分别通过从与血管加压素通透的相同内部储存库(可能是内质网)释放钙离子以及增强该激素引起的细胞外钙离子内流,来加速血管加压素介导的[Ca2+]i升高的快速相并提高平台期。