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Volume-responsive sodium and proton movements in dog red blood cells.
J Gen Physiol 1984 Sep; 84(3):379-401
Coupling between sodium and proton movements in dog red blood cells was investigated directly using the fluorescent probe 3,3'- dipropylthiadicarbocyanine (diSC35) and indirectly by measurement of potassium movements through valinomycin channels. Red blood cells were prepared from fresh blood samples from mongrel dogs and analyzed for sodium, potassium, chlorine, and water content. Membrane hyperpolarization in a choline medium was assessed at hematocrits of 0.33 and 7.4 percent. The membrane potential of the red blood cells was determined before and after cell shrinkage as the external potassium concentration at which there was no change in diSC35 fluorescence. The sodium permeability pathway became progressively activated as the dog red blood cells shrunk below their normal volume. Loss of sodium was inhibited by replacing chlorine with either nitrite or thiocyanate ions. Sodium flux through the membrane occurred in exchange for protons and was inhibited by amiloride. Proton movements were driven by an imposed sodium gradient, and movements of sodium ions were driven by an imposed proton gradient. The large sodium fluxes that occurred in the presence of cell shrinkage were determined to not be conductive in nature. The authors conclude that the sodium/proton exchange mechanism in dog red blood cells activated by cell shrinkage is electroneutrally coupled.
NIOSH-Author; Cell-metabolism; Electrolytes; Laboratory-animals; Erythrocytes; Plasma-membrane; Physiological-response; Cell-function; Cell-biology; Biochemical-analysis; Biological-transport; Biological-distribution
Issue of Publication
Journal of General Physiology
Page last reviewed: May 5, 2020
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