New aspects concerning the 22sodium influx into red cells in essential hypertension.

The different components of the total 22Na influx into red cells (RC) of 21 normotensive subjects and 38 patients with essential hypertension were measured and correlated together. We found that the acceleration of total net 22Na influx in essential hypertension is predominantly caused by an increase of the Na leak and only in a small part effected by an elevated phloretin-sensitive Na countertransport. The 22Na influx mediated by the anion exchange system and the furosemide inhibitable Na-K cotransport were not significantly altered. The correlations suggest that the total 22Na influx into RC of normotensive subjects is very strong and equally defined by both the Na leak and the anion exchange system, whereas an influence of the Na countertransport is not detectable. On the contrary we found a clear decreased dependence upon the anion exchange system in favour of the countertransport in patients with essential hypertension, while the influence of Na leak was unaltered.