Sodium-lithium countertransport activity, external affinity for sodium (kNa) and maximal rate of turnover (Vmax), were characterized in 21 male subjects (aged 45 to 65 years) with angiographically proven coronary artery disease; these were compared with a matched group of healthy controls. No significant differences in countertransport activity were noted between the coronary artery disease patients and the healthy controls. By contrast, the median [range] kNa in the coronary artery disease group (8.5 [2.6 to 30.5] mmol/L Na) was significantly lower than that in the controls (59.9 [5.9 to 240.5] mmol/L Na; P < .0001). This reduction was accompanied by a significantly lower mean Vmax (controls 0.403 +/- 0.187 v coronary artery disease group 0.248 +/- 0.121 mmol Li/L RBC/h; P < .01). The findings suggest that disturbed behavior of the sodium-lithium countertransporter is not confined to hypertension but may represent a broader-based membrane dysfunction associated with vascular disease.

Sodium-lithium countertransport activity has been proposed as a marker for hypertension and is lower in black compared to Caucasian subjects both with and without vascular disease. The question arises of what is the primary kinetic locus of the altered behaviour of the countertransporter in black subjects and whether this is also seen in normotensive subjects from other non-Caucasian ethnic groups.We The clinical and laboratory characteristics of the subjects were similar in all four ethnic groups. Minor differences noted were: significantly higher mean height, weight and serum creatinine concentration (P Ͻ 0.001) and significantly lower plasma triglyceride concentration (P = 0.02) in the black compared to the other

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