[Univalent cation transport in human and rat erythrocytes: its regulation by protein kinase activators and compression].
The effect of the activators of protein kinase A (dibutyryl-cAMP) and protein kinase C (beta-phorbolic ether), as well as cell compression, on the rate of 22Na and 86Rb, a radioactive potassium analogue, incorporation by human and rat erythrocytes was investigated. Protein kinase A and protein kinase C activation was accompanied by the activation of Na+, K+-ATP-ase in human and rat erythrocytes as well as increased Na+, K+ cotransport rate in rat erythrocytes. Human erythrocytes responded to protein kinase C activation by a 2 or 3-fold increase in Na+/Na+-antitransport rate, and both human and rat erythrocytes exhibited a manifold increase in the Na+/H+ metabolism rate. Cell compression depressed Na+, K+-ATP-ase activity and increased the rates of Na+/H+ metabolism and the frusemide-inhibited component of potassium transport, the latter two effects being particularly obvious in rat erythrocytes. It is suggested that protein kinase C activation and/or erythrocyte compression may be a direct cause of increased plasmatic membrane permeability for univalent cations in primary hypertension.
Orlov
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Pokudin
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Postnov
Iu V
IuV
D000818:Animals; D001692:Biological Transport; D003994:Bucladesine / Q000494:pharmacology; D002499:Centrifugation, Density Gradient; D004789:Enzyme Activation / Q000187:drug effects; D004910:Erythrocyte Membrane / Q000378:metabolism*; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D010703:Phorbol Esters / Q000494:pharmacology; D011188:Potassium / Q000493:pharmacokinetics*; D011494:Protein Kinases / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000493:pharmacokinetics*
D010703:Phorbol Esters; D003994:Bucladesine; D012964:Sodium; D011494:Protein Kinases; D011188:Potassium
Transport odnovalentnykh kationov v éritrotsitakh cheloveka i krysy: reguliatsiia aktivatorami proteinkinaz i szhatiem.