Bone as an ion exchange system: evidence for a pump-leak mechanism devoted to the maintenance of high bone K(+).
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(+)](o)), an inward steady current density (7.85-38.53 microA/cm(2)) was recorded at the damage site, which was significantly dependent on [K(+)](o). At [K(+)](o) equal to that of BECF (25 mM), current density was reduced by 76%. At [K(+)](o) 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.
Rubinacci
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A
Bone Metabolic Unit, Scientific Institute H San Raffaele, Milano 20132, Italy. alessandro.rubinacci@hsr.it
Benelli
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FD
Borgo
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E
Villa
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I
D000818:Animals; D017609:Barium Compounds / Q000494:pharmacology; D001842:Bone and Bones / Q000293:injuries / Q000378:metabolism*; D002712:Chlorides / Q000494:pharmacology; D003470:Culture Media / Q000737:chemistry / Q000494:pharmacology; D004553:Electric Conductivity; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005110:Extracellular Space / Q000378:metabolism; D007474:Ion Exchange; D051379:Mice; D009994:Osmolar Concentration; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism* / Q000502:physiology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology*; D019789:Tetraethylammonium / Q000494:pharmacology; D014950:Wounds, Penetrating / Q000378:metabolism
D017609:Barium Compounds; D002712:Chlorides; D003470:Culture Media; D004791:Enzyme Inhibitors; D026902:Potassium Channel Blockers; D015221:Potassium Channels; C024986:barium chloride; D010042:Ouabain; D019789:Tetraethylammonium; D000254:Sodium-Potassium-Exchanging ATPase; D011188:Potassium