Marked Na+/Li+ countertransport hyperactivity and post-load hyperinsulinaemia have been described in 93% of patients with cardiac syndrome X. We hypothesized that more complex abnormalities in Na+ traffic across the cell membrane are present in these patients. The aim of the present study was to evaluate the activities of the two main transporters responsible for transmembrane Na+ transport, i.e. the ATPase-dependent Na+ pump and the Na+–K+–2Cl- co-transporter, in a selected group of patients with cardiac syndrome X. We evaluated 19 patients with cardiac syndrome X and 14 control subjects. The ATPase-dependent Na+ pump and Na+–K+–2Cl- co-transport activities were assessed from Na+-loaded red blood cells by using nystatine, in the presence of furosemide and ouabain, as appropriate. Erythrocyte Na+/Li+ countertransport activity, serum lipid and post-load (75 g of oral glucose) insulin levels were also evaluated. The Vmax of Na+/Li+ countertransport (P = 0.0001) and post-load insulin levels (120 min; P = 0.001) were confirmed to be higher in patients with syndrome X than in controls. The Vmax of Na+–K+–2Cl- co-transport was similar in patients and controls. By contrast, the Vmax of the ATPase-dependent Na+ pump was significantly lower (P = 0.002) in syndrome X patients (3.13±0.87 mmol·h-1·l-1) than in controls (4.28±1.10 mmol·h-1·l-1). Serum total cholesterol and triacylglycerol concentrations were also higher in patients with syndrome X than in control subjects (P < 0.0001). Thus decreased activity of the ATPase-dependent Na+ pump was present in patients with cardiac syndrome X. Such an abnormality has the biological potential to augment microvascular tone and the response to constrictor stimuli via increased intracellular free Ca2+. Of note, syndrome X patients also manifested Na+/Li+ countertransport hyperactivity which, in turn, is known to induce peripheral insulin resistance and consequent abnormalities in insulin secretion and lipid turnover. Thus cardiac syndrome X appears as a multifaceted syndrome presenting with either metabolic or cardiovascular symptoms, or both, based on the expression of complex abnormalities in Na+ traffic across the cell membrane.

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