Erythrocytes from a patient with hypokalemic periodic paralysis (HPP) have been studied, in order to investigate the presence of alterations of membrane cation active transport systems. An original 23Na-NMR method has been used, capable of evaluating quantitatively the Na+ efflux due to the Na+/K+/Cl- cotransport. This method uses a loading system to increase internal cellular Na+ concentration: in the patient with HPP both the internal Na+ concentration after loading and the Na+/K+/Cl- cotransport activity were decreased in comparison to the controls. Our data seem to confirm that the fall of K+ serum levels during attacks in HPP must be ascribed to a shift of K+ from extra- to intracellular compartment (with consequent changes in the fibrocellular membrane polarity), due to an alteration of membrane cation transport system: which does not only consist in a hyperactivity of Na+/K+ ATPase (already described by other AA.), but also in a "secondary" decreased K+ efflux driven by the cotransport. The decrease of cotransport activity may be considered as "compensatory" (in fact, the intracellular Na+ content is normal), since this transport system can work as a kind of "emergency" system that can "help" the ATPase-dependent pump in extruding any excess of cell Na+ content, or can be depressed by any decrease of this value, caused by an hyperactivity of the Na+/K+ ATPase. The decreased cotransport activity results in a powerful contribution to the increase of intracellular potassium due to the hyperactivity of the Na+/K+ pump. This method could supply a useful diagnostic marker in all uncertain cases.