A further characterization of the selective K movements observed in human red blood cells following acetylphenylhydrazine exposure.
Following brief exposure to acetylphenylhydrazine, the potassium permeability of the human erythrocyte membrane is selectively augmented. While a similar increase in potassium permeability results from the intracellular accumulation of calcium (the Gardos phenomenon), we have found a number of features that allow these two pathways to be distinguished from one another. The acetylphenylhydrazine pathway does not require calcium for its activation, and can be seen even in the presence of a molar excess of the calcium chelator EGTA. The transmembrane potassium movement via this channel has a specific requirement for the anion chloride, and it can be inhibited by furosemide. The potassium that moves through the Gardos pathway, on the other hand, can be accompanied by any permeant anion, and is inhibitable by quinidine or cetiedil. Thus, acetylphenylhydrazine exposure seems to promote K + Cl cotransport, whereas the Gardos pathway represents a potassium conductive channel. While full demonstration of both these pathways requires harsh in vitro manipulation, the large electrochemical potassium gradient favoring the movement of this cation out from the erythrocyte suggests that even a partial activation of either pathway could cause intracellular dehydration and thus contribute importantly to the pathophysiology of in vivo red cell destruction.
D002463:Cell Membrane Permeability / Q000187:drug effects; D003681:Dehydration; D004910:Erythrocyte Membrane / Q000187:drug effects*; D005665:Furosemide / Q000494:pharmacology; D006801:Humans; D010659:Phenylhydrazines / Q000494:pharmacology*; D011188:Potassium / Q000097:blood*
D010659:Phenylhydrazines; D005665:Furosemide; C006384:N(1)-acetylphenylhydrazine; D011188:Potassium