The Li-Na exchange in red cells of essential hypertensive patients with low Na-K cotransport.

Abstract

Impairments of sodium-potassium (Na-K) cotransport and lithium-sodium (Li-Na) countertransport have been reported in essential hypertension. The Vmax of Li-Na countertransport was measured in Li-loaded cells (9 mmol/l cells) by determining the external Na-stimulated Li efflux. Countertransport was measured in 29 normotensive subjects without a family history of hypertension (NT -FHH), 22 normotensive subjects with a family history of hypertension (NT +FHH) and 45 essential hypertensive patients (HT) [mean +/- s.d.: 348 +/- 138 (NT -FHH), 397 +/- 133 (NT +FHH) and 456 +/- 166 (HT)]. There was no significant elevation of Li-Na countertransport in the hypertensive group with respect to NT -FHH. The outward Na-K cotransport was measured in Na-loaded cells (Na greater than 25 mmol/l cells) by determining the frusemide-sensitive Na efflux. Na-K cotransport was found to be significantly decreased in the hypertensive patients compared to the normotensive controls [mean +/- s.d.:280 +/- 136 (HT) and 424 +/- 128 (NT -FHH)]. The present collaborative study between the two laboratories revealed that the fraction of patients with an alteration in the Vmax of cotransport or countertransport was different in the two laboratories and could not be accounted for by any methodological or experimental procedure. This study shows that different patterns of transport impairments might occur in different populations, thus suggesting a heterogeneity of cation transport alterations in hypertensives.