Sodium Transport in Human Platelets as an Index of Na,K-ATPase Activity

Abstract

Both sodium ((22)Na) and rubidium ((86)Rb) influx, an index of potassium transport, were studied in human platelets to establish a simple and rapid method for the study of the sodium pump in platelets. (22)Na was taken up by platelets in a time dependent manner. Ouabain, an inhibitor of the sodium pump, significantly (p < 0.03) increased intracellular (22)Na content. Adrenaline significantly (p < 0.02) increased (22)Na content initially. This adrenaline-induced increase did not occur in the presence of ouabain. Timolol (a β(1),β(2)-adrenoceptor antagonist) but not atenolol (a β(1),-adrenoceptor antagonist) inhibited these adrenaline-induced responses. Xamoterol (a β(2) -adrenoceptor agonist) did not cause an increase in platelet (22)Na content and unexpectedly, nor did salbutamol (a pVadrenoceptor agonist). BRL 37344 (an 'atypical' β(3)-adrenoceptor agonist) caused a significant (p < 0.002) increase in platelet (22)Na content that was significantly (p < 0.02) inhibited by timolol. Active (86)Rb influx was significantly (p < 0.02) stimulated by salbutamol. BRL 37344 also significantly (p < 0.005) stimulated active (86)Rb influx; this process was inhibited by timolol. There are considerable similarities between (22)Na and (86)Rb transport in the human platelet. The only discrepancy, with salbutamol, may be due to methodological sensitivity or to different factors controlling the transport of these two ions. The findings of the present study indicate that it may be necessary to assess both (22)Na and (86)Rb transport in order to make conclusions concerning the sodium pump, in human platelets.