Role of intracellular sodium in the hypertension of pre-eclampsia - abstract

ABSTRACT

Patients with pre-eclampsia have abnormal sodium homeostasis. This is so at the level of the whole body as well as at a cellular level. We have described in such patients raised leucocyte sodium content and lowered potassium which are probably related to slowing of the sodium pump (Forrester and Alleyne, 1980, Clinical Science 59 199-201). In order to investigate whether the abnormal cell sodium content was causally related to blood pressure elevation, we prospectively measured leucocyte sodium content and blood pressure in 85 obstetrically normal primigravidae. Seven developed pre-eclampsia. In these patients both blood pressure and cell sodium rose pari passu up to delivery and fell post partum. A similar but smaller trend was seen in controls. Thus pre-eclampsia was associated with exaggerated changes in cell sodium content which paralleled blood pressure changes. Cell potassium content fell in both groups but to a greater extent in pre-eclamptics. (Seon and Forrester, 1988, Clinical Science 75 in press). Patients who developed pre-eclampsia had higher blood pressure and cell sodium at six weeks post partum, suggesting that the pregnancy changes had not fully resolved. We therefore cross-sectionally measured blood pressure and leucocyte sodium content in patients who had had pre-eclampsia and delivered 40 weeks previously and compared them with matched controls (Forrester et al, Clinical Science, in press). Raised intracellular sodium can cause high blood pressure by raising peripheral resistance. We propose that this is a probable mechanism for blood pressure changes in pre-eclampsia (AU)