Abstract
Recent demonstrations of chloride-associated passive potassium movements in red blood cells of humans, ducks, sheep, and toadfish prompted a reinvestigation of potassium permeability in dog red blood cells. Early observations of Davson (J. Physiol. London 101:265-283, 1942) had shown that replacement of chloride by nitrate and thiocyanate caused a greatly increased rate of potassium flux across the dog red cell membrane. This finding seemed at variance with results in other species in which chloride replacement caused a fall in potassium flux. The present data indicate that passive potassium movements in swollen dog red blood cells are chloride dependent and furosemide sensitive, as shown for the cells of other species. Davson's findings were demonstrated to be due to the inclusion of small quantities of calcium in the medium under circumstances that favored calcium entry into the cells, thus opening the calcium-activated potassium channel described by Gardos (Curr. Top. Membr. Transp. 10:217-277, 1978 and Nature London 279:248-250, 1979). Potassium movements through the latter channel were stimulated when chloride was replaced by more permeant anions, such as nitrate and thiocyanate, which also increased the rate of net potassium movements in valinomycin-treated cells.
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