Schweigel M, Martens H
Institut für Veterinär-Physiologie der Freien Universität Berlin.
Berl Munch Tierarztl Wochenschr. 2000 Mar;113(3):97-102.
The forestomach is the main site of Mg2+ absorption in the gastrointestinal tract of ruminants and maintains Mg2+ homeostasis. It has long been known that an increase in K+ intake and, consequently, in ruminal K+ concentration ([K+]) decreases the apparent digestibility of Mg2+, which increases the risk of hypomagnesemia and tetany. The present review summarizes new findings on the mechanisms of Mg2+ absorption across the rumen epithelium. It has been shown that transcellular and active Mg2+ transport is the predominant pathway for Mg2+ transport from lumen to blood. It is well established that the apical uptake of Mg2+ is mediated by a PD-independent of K(+)-insensitive and by a parallel working PD-dependent, K+ sensitive mechanisms. The predominant driving force for the electro-diffusive Mg2+ uptake is PDa, the potential difference across the apical membrane of the rumen epithelium, that amounts to -50 mV under physiological conditions, permitting an effective Mg2+ absorption even at very low luminal Mg2+ concentrations. The antagonism between K+ and Mg2+ absorption can be explained by K+ dependent electrophysiological changes of the rumen epithelium. An elevation of the ruminal [K+] has two different effects that are responsible for the observed reduction of net Mg2+ absorption; (1) It depolarizes PDa and thereby reduces the driving force for the electro-diffusive Mg2+ uptake into the ruminal epithelial cells, hence decreases the cytosolic [Mg2+] and the transcellular component of Mg2+ absorption; (2) It increases the transepithelial potential difference (PDt; blood-side positive) and, hence causes a small, passive backflow of Mg2+ via the paracellular route from the blood side into the lumen. The second, PD-independent uptake mechanism is primarily working at high ruminal [Mg2+]. Therefore the negative effect of K+ can be compensated by this K+ insensitive Mg2+ absorption, if high [Mg2+] are present in the ruminal fluid.
前胃是反刍动物胃肠道中镁离子吸收的主要部位，并维持镁离子的体内稳态。长期以来，人们已知钾摄入量增加，进而瘤胃液中钾离子浓度（[K⁺]）升高，会降低镁的表观消化率，这增加了低镁血症和搐搦的风险。本综述总结了瘤胃上皮镁离子吸收机制的新发现。研究表明，跨细胞主动转运镁离子是镁离子从管腔转运至血液的主要途径。众所周知，镁离子的顶端摄取由一种不依赖钾离子、对钾离子不敏感的途径以及一种与之并行的依赖钾离子、对钾离子敏感的途径介导。电扩散性镁离子摄取的主要驱动力是瘤胃上皮顶端膜两侧的电位差（PDa），在生理条件下其值为 -50 mV，即使在管腔镁离子浓度非常低时也能实现有效的镁离子吸收。钾离子与镁离子吸收之间的拮抗作用可通过瘤胃上皮依赖钾离子的电生理变化来解释。瘤胃液中[K⁺]升高有两种不同作用，导致观察到的镁离子净吸收减少：（1）它使PDa去极化，从而降低电扩散性镁离子摄取进入瘤胃上皮细胞的驱动力，进而降低细胞内[Mg²⁺]和镁离子吸收的跨细胞成分；（2）它增加跨上皮电位差（PDt；血液侧为正），因此导致少量镁离子通过细胞旁途径从血液侧被动回流到管腔。第二种不依赖电位差的摄取机制主要在瘤胃液中高镁离子浓度时起作用。因此，如果瘤胃液中存在高浓度的镁离子，这种对钾离子不敏感的镁离子吸收可补偿钾离子的负面影响。
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