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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.

We have studied the relationship between sodium-lithium countertransport, determined in childhood, and family history of hypertension. Countertransport was measured in healthy children and those with secondary hypertension. There was no significant difference in countertransport between these two groups. In the normal children (n = 52, median age 6.8 years), there was a positive relationship between body mass index and countertransport (rs = 0.34, p < 0.02). A positive relationship between family history of hypertension using a ranked scoring system, and countertransport, not related to age, body mass or blood pressure (n = 34, rs = 0.63, p < 0.001) was also found. There was no significant relationship between intracellular sodium concentration and countertransport. These data confirm that countertransport in normal children is related to body mass index and indicate that a genetic predisposition to primary hypertension marked by sodium-lithium countertransport is identifiable in childhood.

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.

1. Erythrocytic sodium-lithium (Na-Li) countertransport (CT) was measured in normotensive Maori and non-Maori by in vitro and in vivo methods to determine its relationship to erythrocytic hypernatraemia previously identified in Maori. 2. In vivo and in vitro CT rates were correlated within race and were similar between races. Countertransport rate was correlated with erythrocytic sodium concentration only in Maori. 3. The findings suggest the possibility of a genetically determined alteration in CT stoichiometry in Maori.

Objective To establish the changes in erythrocyte sodium lithium countertransport (SLC) with advancing normal pregnancy and to determine if these changes were different in pregnancy induced hypertension (PIH). The changes in both groups were assessed in relation to haemodynamic changes. Design SLC, mean arterial pressure (MAP), cardiac output (CO) and total peripheral vascular resistance (TPVR) were determined serially during normal pregnancy and cross-sectionally in PIH. Women were studied again 20 weeks after delivery where possible. Setting Routine antenatal clinic and antenatal ward of a regional reference centre. Subjects Fifty-one normal primigravid women were studied serially and 41 primigravid women with PIH were studied at time of diagnosis. Results During normal pregnancy SLC (mmol Li/h/l cells) increased from a nonpregnant value of 0.24 ± 0.02 (mean ± SEM) to 0.32 ± 0.02 at 14 weeks, and 0.37 ± 0.02 at 20 weeks gestation. This was maintained until 38 weeks (0.40 ± 0.02). The increase until 20 weeks occurred at the time of greatest change in CO (5.10 ± 0.18 to 6.79 ± 0.20 l/min) and TPVR (1327 ± 58 to 969 ± 33 dyn/s/cm−5). The decrease in TPVR with a rise in SLC is opposite to the relation reported in essential hypertension so that a functional relation is unlikely. However, the changes within pregnancy were positively correlated (r = 0.43, P

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.

The rate of sodium-lithium countertransport (SLC flux) across red cell membranes has been reported to be elevated in hypertensive persons and their relatives as compared to normotensive individuals without family histories of hypertension. We have investigated the inheritance of this trait in 434 persons from 10 kindreds. Relatives show positive correlation of SLC flux values, but there is no spouse-spouse correlation. Pedigree analysis favors a model of polygenic inheritance over models of major-gene inheritance. Major-gene index statistics and offspring-between-parent statistics provide similar results. The proportion of total pheno-typic variance that is attributable to polygenic differences between persons is estimated at 71%. The SLC flux values of hypertensive persons in this study population are lower than those reported from Boston, but are similar to those reported from Europe. We found a broad overlap of SLC flux values for hypertensive and normotensive persons. We conclude that SLC flux probably is not useful as a preclinical marker for essential hypertension.