Rubinacci A, Benelli F D, Borgo E, Villa I
Bone Metabolic Unit, Scientific Institute H San Raffaele, Milano 20132, Italy.
Am J Physiol Endocrinol Metab. 2000 Jan;278(1):E15-24. doi: 10.1152/ajpendo.2000.278.1.E15.
To provide evidence of active accumulation of K(+) in bone extracellular fluid (BECF), electric currents driven by damaged living metatarsal bones of weanling mice, immersed in physiological media at different [K(+)], in the presence of blockers of the K(+) channels or of the Na(+)-K(+-)ATPase inhibitor, were measured by means of a voltage-sensitive two-dimensional vibrating probe. At 4 mM extracellular K(+) concentration (K(+)), an inward steady current density (7.85-38.53 microA/cm(2)) was recorded at the damage site, which was significantly dependent on K(+). At K(+) equal to that of BECF (25 mM), current density was reduced by 76%. At K(+) of 0 mM, the current density showed an increase, which was hindered by tetraethylammonium (TEA). Basal current density was reduced significantly after exposure to TEA or BaCl(2) and was unchanged after long- term exposure to ouabain. By changing control medium with a chloride-free medium, current density was reversed. The results support the view that K(+) excess in bone is maintained by a biologically active cellular system. Because the osteocyte-bone lining cell syncytium was at the origin of the current in bone, it is likely that this system controls the ionic composition of BECF.
为了提供钾离子（K⁺）在骨细胞外液（BECF）中主动积累的证据，将断奶小鼠的受损活体跖骨浸入不同钾离子浓度（[K⁺]）的生理介质中，在存在钾离子通道阻滞剂或钠钾ATP酶抑制剂的情况下，通过电压敏感二维振动探针测量其驱动的电流。在细胞外钾离子浓度（[K⁺]ₒ）为4 mM时，在损伤部位记录到内向稳定电流密度（7.85 - 38.53微安/平方厘米），该电流密度显著依赖于[K⁺]ₒ。当[K⁺]ₒ等于BECF中的浓度（25 mM）时，电流密度降低了76%。在[K⁺]ₒ为0 mM时，电流密度增加，而四乙铵（TEA）可抑制这种增加。暴露于TEA或氯化钡后，基础电流密度显著降低，而长期暴露于哇巴因后电流密度不变。用无氯介质替换对照介质后，电流密度发生逆转。这些结果支持了骨中钾离子过量由生物活性细胞系统维持的观点。由于骨细胞 - 骨衬细胞合体是骨中电流的起源，这个系统很可能控制着BECF的离子组成。
