Restoration of a Potassium-requiring Sodium Pump in Squid Giant Axons Poisoned with CN and Depleted of Arginine

Abstract

MICROINJECTION of high energy phosphate compounds such as ATP and phosphoarginine (ArgP) into CN-poisoned squid giant axons restores sodium extrusion to normal levels¹. Only the latter compound, however, also restores the “K-free effect”, that is to say, a 30–70 per cent drop in sodium efflux when the axon is transferred to potassium-free seawater². Furthermore, treatments resulting in intracellular ArgP breakdown without ATP breakdown (namely, incipient CN poisoning or partial poisoning with 2,4-dinitrophenol) abolish the K-free effect. Caldwell et al.³ considered two possible explanations for this observation: either ArgP itself plays a part in Na–K coupling, or a high axoplasmic ATP/ADP ratio is required for the K-free effect to occur. Injected ArgP continuously regenerates ATP from ADP, maintaining a high ratio, whereas injected ATP rapidly breaks down to ADP, thus lowering the ratio.