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On the basis of a preliminary observation that sodium-lithium countertransport showed different intra-individual variations when calculated by two standard methods despite using the same sets of lithium efflux data, we decided to compare values by the two methods in a much larger number (50) of volunteers. Although there was significant correlation between the two sets of values (r = 0.936), mean value by M-1 was significantly higher than that by M-2 (P < 0.007). Using appropriate statistical methodology, the limits of agreement between M-1 and M-2 values (-0.066 to 0.096 mmol L cell-1 h-1) were considerable; and the 95% confidence limits of the bias (i.e. mean difference) did not include zero. Furthermore, neither the 95% confidence interval for the correlation coefficient nor that for the slope of regression line included 1.0. These suggest lack of agreement between the two sets of values. The probable cause of this difference is discussed.

Inheritance is a major determinant of increased sodium-lithium countertransport (SLC) activity in hypertension. However, hyperlipidaemia can also cause increased SLC activity in some individuals and it is difficult to distinguish this effect from the effect of hypertension. Erythrocyte SLC activity and its kinetic determinants sodium affinity (km) and maximum velocity (Vmax) were measured in 25 hyperlipidaemic patients and 15 normal controls (NC). Increased SLC activity (0.31 +/- SEM 0.03 mmol Li/(h x 1 cells) vs. NC 0.20 +/- 0.01, P < 0.01) in the hyperlipidaemic patients was associated with increased Vmax (0.59 +/- 0.07 vs. NC 0.41 +/- 0.03, P < 0.01) but normal km (median 120 range [40-324] mmol l-1 vs. 140 [108-260]. Lipid-lowering therapy resulted in decreased SLC activity secondary to a fall in Vmax. Km remained constant despite the changes in lipids and Vmax. The mechanism of increased SLC activity in hyperlipidaemia is different from that in essential hypertension where increased sodium affinity is found. Measurement of the kinetic characteristics of SLC may discriminate between the independent influences of hypertension and hyperlipidaemia on the sodium-lithium countertransporter.

Sodium lithium countertransport may be a genetic marker for arterial hypertension and for the risk of diabetic nephropathy in type 1 diabetic patients. Since various factors seem to influence the transport velocity including serum lipid alterations, erythrocytes of seven patients with severe hyperlipoproteinaemia who were chronically and intermittently treated with LDL apheresis were examined before and immediately after therapy. The LDL apheresis reduced sodium lithium countertransport significantly (0.383 vs 0.269, P less than 0.02). Therefore, we conclude that serum lipid composition must be considered when interpreting sodium lithium countertransport velocity.

Sodium-lithium countertransport (Na-Li CT) has been reported to be increased in essential hypertension (EHT) but the nature and degree of distinction from normal controls is unclear. Of 44 unselected patients with EHT in the hospital hypertension clinic 36% had Na-Li CT greater than the normal control range and 70% of these had a family history of hypertension. Almost all the patients with normal Na-Li CT had no family history of hypertension. Analysis of variance showed that raised Na-Li CT was related to both a family history of hypertension and a family history of a cardiovascular event. Of 23 patients with hypertension secondary to renal disease, 43% had Na-Li CT greater than the normal control range and raised Na-Li CT was related to both a family history of hypertension and a family history of cardiovascular event in the same way as EHT. Raised Na-Li CT was not characteristic of EHT but identified a subgroup of patients with EHT and a family history of hypertension, some of whom also had renal disease.

It has recently been found that the Na+-Li+ countertransport across the human erythrocyte membrane is increased in patients with essential hypertension. We investigated the influence of hypokalaemia, oral contraceptives, diabetes mellitus and essential hypertension on the activity of this transport system. Normal values for the maximal Na+-Li+ transport rate were 0.25 +/- 0.08 mmol l-1 h-1 (males, n = 18) and 0.23 +/- 0.06 (females, n = 14). We found elevated values in women taking oral contraceptives (0.34 +/- 0.07, n = 10, P less than 0.001), in patients with chronic hypokalaemia due to diuretic or laxative abuse (0.41 +/- 0.16, n = 13, P less than 0.005) and in those with essential hypertension (0.32 +/- 0.08, n = 24, P less than 0.001) (all data mean +/- SD). Thus our results with hypertensive patients support the findings of other investigators. However, oral contraceptives and drug-induced hypokalaemia greatly modify this system, indicating a regulation of the Na+-Li+ countertransport by hormones. Thus the transport rate does not seem to be an appropriate test for the diagnosis of essential hypertension.