CALCIUM-SENSITIVE CELLULAR AND SUBCELLULAR TRANSPORT OF SODIUM, POTASSIUM, MAGNESIUM, AND CALCIUM IN SODIUM-LOADED VASCULAR SMOOTH-MUSCLE - ELECTRON-PROBE ANALYSIS

Electron probe x-ray microanalysis of the composition of rabbit portal anterior mesenteric vein smooth muscle was performed following sodium loading and washout into sodium-free lithium solutions. Sodium and lithium were also measured with atomic absorption spectrophotometry. Cellular uptake of sodium and loss of potassium during sodium loading were much faster at high (37.degree. C) than at low (2 .degree. C) temperature, as was the passive ouabain-resistant uptake of potassium during lithium washout. The loss of sodium at 2.degree. C into lithium solution consisted of two components: a rapid efflux that was complete by 30 minutes, and a slow component that required at least 24 hours for completion. The amount of sodium lost through the first component (approximately 200-300 mmol/kg dry weight) was relatively independent of the amount of sodium loading. The loss of cellular sodium at 2.degree. C, after 30 minutes, was accompanied by a gain of cellular lithium. Ouabain-resistant sodium loss and lithium and potassium uptake were markedly accelerated at 37.degree. C; sodium loss was complete (1200 mmol sodium/kg dry weight lost) by 30 minutes of washout. Sodium-loaded cells also lost chloride ion and gained magnesium during sodium efflux at 37.degree. C. Mitochondrial and nuclear sodium and potassium were correlated with the respective cytoplasmic concentrations during both sodium loading and sodium washout, indicating the relatively rapid equilibration of the monovalent ions between the cytoplasm and organelles. Calcium-free solutions markedly inhibited the ouabain-resistant sodium and chloride ion effluxes and potassium influx in muscles incubated, after sodium loading, in lithium solutions at 37.degree. C. These fluxes could be restored to near normal values by 0.2 mM calcium. The calcium sensitivity of the ouabain-resistant sodium, potassium, and chloride ion fluxes observed in this and other studies raises the possibility that some abnormalities of monovalent ion transport observed in cells of hypertensives are secondary to changes in cellular calcium.