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β-肾上腺素能儿茶酚胺对虹鳟(Salmo gairdneri)红细胞中细胞体积和离子转运的调控

Control of cell volume and ion transport by beta-adrenergic catecholamines in erythrocytes of rainbow trout, Salmo gairdneri.

作者信息

Borgese F, Garcia-Romeu F, Motais R

出版信息

J Physiol. 1987 Jan;382:123-44. doi: 10.1113/jphysiol.1987.sp016359.

Abstract
  1. Trout red cells suspended in an isotonic medium containing beta-adrenergic catecholamines or adenosine 3',5'-phosphate (cyclic AMP) enlarge rapidly to reach a new steady-state volume which is maintained as long as hormone is present. The volume response is not changed by inhibition of the Na+-K+ pump with ouabain. The new steady-state volume was shown to result from a dynamic equilibrium involving the simultaneous functioning of two regulatory processes induced by hormone: a volume increase response that causes cells to enlarge by gaining Na+ and a volume decrease response that causes cells to shrink by losing K+. 2. As previously described, the volume increase response due to NaCl entry, is mediated by the activation by cyclic AMP of a Na+-H+ antiport operating in parallel to Cl(-)-OH- exchanges. In addition, it is shown in this paper that the Na+ uptake is a discontinuous, oscillatory process and that NaCl entry continues for several hours, i.e. as long as hormone is present. 3. The volume decrease response involves a passive, Cl(-)-dependent K+ loss. Na+ cannot use this pathway. The response is blocked by replacement of Cl- by NO3-, by loop diuretics (furosemide, bumetanide) but also by inhibitors of the anion exchanger (4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), niflumic acid). The activation of this ouabain-insensitive, Cl(-)-dependent K+ transport system is not directly triggered by cyclic AMP. It involves an all-or-none type of switching phenomenon which occurs when the cells swell to a certain volume. Thus it is a regulatory response to the increase in cell volume induced by stimulation of the Na+-H+ exchange by cyclic AMP. Inactivation is also volume dependent: when the cell size approaches the initial size the pathway shuts off. Thus the controlling mechanism of the K+ pathway acts like a reversible on-off switch that operates around a given volume. Ca2+ was not found to be involved in this control. Cyclic AMP is not necessary to keep the activated K+ pathway open but it could be one of the factors involved in the activating process. 4. There are several lines of evidence indicating that in trout red cells the volume decrease and the volume increase responses may not be brought about by the same transport mechanism operating in different modes. The movements of Na+, K+ and Cl- account for the water movements during volume increase and decrease. Thus movements of other solutes such as amino acids need not be considered.
摘要
  1. 悬浮于含有β-肾上腺素能儿茶酚胺或3',5'-磷酸腺苷(环磷酸腺苷)的等渗介质中的虹鳟红细胞会迅速膨胀,达到一个新的稳态体积,只要激素存在,该体积就会维持不变。用哇巴因抑制钠钾泵并不会改变体积反应。新的稳态体积是由一种动态平衡导致的,这种平衡涉及激素诱导的两个调节过程的同时作用:一个是体积增加反应,通过摄取钠离子使细胞膨胀;另一个是体积减少反应,通过丢失钾离子使细胞收缩。2. 如前所述,由氯化钠进入引起的体积增加反应是由环磷酸腺苷激活的钠氢反向转运体介导的,该转运体与氯氢氧根交换并行运作。此外,本文还表明,钠离子摄取是一个不连续的振荡过程,并且氯化钠的进入会持续数小时,即只要激素存在就会持续。3. 体积减少反应涉及一种依赖氯离子的被动钾离子丢失。钠离子不能通过这条途径。用硝酸根取代氯离子、使用袢利尿剂(呋塞米、布美他尼)以及阴离子交换抑制剂(4,4'-二异硫氰酸芪-2,2'-二磺酸(DIDS)、尼氟灭酸)均可阻断该反应。这种对哇巴因不敏感、依赖氯离子的钾离子转运系统的激活并非直接由环磷酸腺苷触发。它涉及一种全或无类型的开关现象,当细胞膨胀到一定体积时就会发生。因此,这是对环磷酸腺苷刺激钠氢交换所诱导的细胞体积增加的一种调节反应。失活也依赖于体积:当细胞大小接近初始大小时,该途径就会关闭。因此,钾离子途径的控制机制就像一个可逆的开关,围绕给定体积运作。未发现钙离子参与这种控制。环磷酸腺苷并非维持激活的钾离子途径开放所必需,但它可能是参与激活过程的因素之一。4. 有几条证据表明,在虹鳟红细胞中,体积减少和体积增加反应可能并非由以不同模式运作的相同转运机制引起。钠离子、钾离子和氯离子的移动解释了体积增加和减少过程中的水分移动。因此,无需考虑其他溶质如氨基酸的移动。

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