SULFHYDRYL-GROUP CONTROL OF SODIUM-LITHIUM COUNTERTRANSPORT KINETICS - A MEMBRANE-PROTEIN CONTROL ABNORMALITY IN ESSENTIAL-HYPERTENSION

Erythrocyte sodium-lithium countertransport (SLC) is an obligatorily c oupled equimolar exchange of intracellular sodium or lithium with extr acellular sodium or lithium. SLC is partially inhibited by N-ethylmale imide (NEM) but only when a transported ion (sodium or lithium) is pre sent in the extracellular medium. In essential hypertensive patients w ith a strong family history of hypertension the Km of SLC for extracel lular sodium was lower and Vmax tended to be higher than in normal con trols, but the ratio Vmax/Km gave a much clearer distinction between t he two groups. After NEM treatment, the remaining SLC activity in norm al individuals had a lower Vmax and Km for sodium but Vmax/Km was not affected. In essential hypertensives the remaining SLC activity after NEM again had lowered Vmax and Km but in these patients the Vmax/Km wa s much lower than in untreated erythrocytes and was then the same as i n normal controls. On the assumption that NEM reacts with a -SH group on a membrane protein that regulates SLC, and that the ratio Vmax/Km r eflects a rate constant for binding extracellular sodium to the unload ed carrier, the results suggest that (a) essential hypertensives have an increased rate of sodium binding to the transporter and (b) this is due to abnormal behaviour of a membrane -SH group.