Abstract

Background: Hypertension that develops after 20 gestational weeks and is defined as pregnancy-induced hypertension (PIH). The main cause of PIH is vasoconstriction and the thickening of vascular media, which decreases vascular capacity and increases peripheral resistance. One of the theories postulated to explain this phenomenon is that a transmembrane sodium transport disorder causes an increase in intracellular sodium concentration. In the latest literature, special attention is paid to the role of the increased intracellular sodium concentration in the pathogenesis of essential hypertension (EH). One of the best documented phenotypes for EH is the increased activity of the sodium-proton exchanger (NHE). The aim of this study was to assess if increased NHE activity could be the mechanism responsible for the development of PIH. Subjects and methods: The study included 30 women: 10 pregnant women with PIH after gestational week 30, 10 women with physiological pregnancy after 30 gestational weeks, and 10 healthy non-pregnant women. NHE activity was determined according to Orlov’s method as amiloride-sensitive H+ efflux from acid-loaded cells. Results: The NHE activity in the group of women with PIH was significantly higher than that in women with physiological pregnancy: 10.09 ± 1.65 vs. 6.81 ± 2.3 mmol/L RBC/h (p < 0.049) and in the group of non-pregnant women: 10.09 ± 1.65 vs. 7.56 ± 1.66 mmol/L RBC/h (p < 0.029). Erythrocyte NHE activity did not differ in the group of women with physiological pregnancy and in the group of non-pregnant women. Conclusion: These results seem to suggest that erythrocyte NHE activity is elevated in PIH pregnancies.

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