Effect of β-Adrenergic Catecholamines on Sodium Transport in Turkey Erythrocytes

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Abstract Sodium fluxes across the plasma membrane of turkey erythrocytes are 2 to 3 times greater than corresponding fluxes in human erythrocytes. Extracellular potassium stimulates fractional sodium outflux and inhibits sodium influx in turkey erythrocytes. In contrast to human erythrocytes, turkey erythrocytes showed no evidence for sodium-sodium exchange, and at all sodium concentrations studied addition of extracellular potassium inhibited sodium influx. Isoproterenol stimulated accumulation of cyclic adenosine 3':5'-monophosphate (cyclic 3':5'-AMP) and produced a 2- to 4-fold increase in sodium fluxes in turkey erythrocytes. The potency of catecholamine analogs for stimulation of sodium transport correlated directly with their potency for activation of adenylate cyclase in the turkey erythrocyte membrane. Stimulation of sodium transport by isoproterenol is reproduced by adding cyclic 3':5'-AMP to the medium and is blocked by propranolol. The increase in cyclic 3':5'-AMP in response to isoproterenol progresses unimpaired for at least 2 hours. The increase in sodium transport, however, begins to diminish within 30 min after addition of isoproterenol, and after 3 hours of incubation sodium fluxes are only slightly greater than for the control. This phenomenon presumably reflects accumulation of an inhibitor or depletion of a necessary factor for the transport system activated by intracellular cyclic 3':5'-AMP. The rapid effect described here of catecholamines on sodium transport as well as certain results with other systems controlled by hormones through cyclic 3':5'-AMP suggest that endocrine regulation of sodium transport is of general biological significance.