Effect of metabolic inhibitors on K+ transport across the lamprey (Lampetra fluviatilis) erythrocyte membrane.
In order to assess the contribution of oxidative metabolism to K+(86Rb+) transport across the lamprey red cell membrane, the effects of various metabolic inhibitors were examined. The influx of K+ was reduced markedly in the presence of 20 mumol/l 2,4-dinitrophenol (2,4-DNP) or rotenone, and to a lesser extent by 1 mmol/l cyanide. Rotenone produced complete inhibition of the K+ active transport and a partial blockade of K+ channels by 28% on the average. Addition of 2,4-DNP to incubation media resulted in a significant reduction of both active transport of K+ (by 47%) and of K+ movement via channels (by 57%). The inhibitory effect of 2,4-DNP on total K+ influx was independent on decreasing extracellular pHe from 7.4 to 6.5. The blocking action of 1 mmol/l Ba2+ on K+ channels was abolished in the red cells incubated at pHe 6.5. Treatment of the red cells with 1 mmol/l cyanide diminished active transport of K+ to about 34% of control values but did not affect K+ channels. The obtained data indicate that in the lamprey red blood cells at least a half of energy needed for the active transport of K+ is supplied with ATP produced by oxidative phosphorylation. It may be suggested that NADH dehydrogenase is the key enzyme required for active transport of K+ in the cells, as rotenone, a selective blocker of this enzyme, causes a complete blockade of the Na+, K(+)-pump.
Gusev
G P
GP
Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg.
Sherstobitov
A O
AO
D019297:2,4-Dinitrophenol; D000818:Animals; D000963:Antimetabolites / Q000494:pharmacology*; D001464:Barium / Q000494:pharmacology; D004140:Dinitrophenols / Q000494:pharmacology; D004910:Erythrocyte Membrane / Q000187:drug effects* / Q000378:metabolism*; D005260:Female; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D017136:Ion Transport / Q000187:drug effects; D007798:Lampreys; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D010085:Oxidative Phosphorylation; D011188:Potassium / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D011803:Quinine / Q000494:pharmacology; D012402:Rotenone / Q000494:pharmacology; D012413:Rubidium / Q000493:pharmacokinetics; D012966:Sodium Cyanide / Q000494:pharmacology
D000963:Antimetabolites; D004140:Dinitrophenols; D015221:Potassium Channels; D012402:Rotenone; D001464:Barium; D010042:Ouabain; D011803:Quinine; D012413:Rubidium; D012966:Sodium Cyanide; D019297:2,4-Dinitrophenol; D011188:Potassium