Sodium-renin-aldosterone relations in normal and hypertensive pregnancy
Article first published online: 19 AUG 2005
DOI: 10.1111/j.1471-0528.1988.tb06812.x
Issue
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BJOG: An International Journal of Obstetrics & Gynaecology
Volume 95, Issue 12, pages 1237–1246, December 1988
Additional Information
How to Cite
BROWN, M. A., NICHOLSON, E. and GALLERY, E. D. M. (1988), Sodium-renin-aldosterone relations in normal and hypertensive pregnancy. BJOG: An International Journal of Obstetrics & Gynaecology, 95: 1237–1246. doi: 10.1111/j.1471-0528.1988.tb06812.x
Publication History
- Issue published online: 19 AUG 2005
- Article first published online: 19 AUG 2005
- Received 16 November 1987, Accepted 30 March 1988
- Abstract
- References
- Cited By
Summary. To examine the short-term regulation of sodium excretion, plasma volume, and the renin-aldosterone system in pregnancy, women in their first pregnancy received either a high-salt (HS) (250 mmol/day) or a low-salt (LS) (20 mmol/day) diet for 7 days during the second and third trimester and after delivery (total 213 studies). Twenty women, studied while normotensive during mid-pregnancy, developed pregnancy-induced hypertension (PIH) in the third trimester. There was slightly greater difficulty adapting to sodium depletion (LS diet) during normal pregnancy compared with postpartum. The final mean values for sodium excretion were 27 (SE 2), 28 (SE 3) and 14 (SE 4) mmol/day in the second and third trimester and postpartum respectively. Sodium excretion with the HS diet was similar at all stages and plasma volumes were maintained as effectively during pregnancy as after delivery following both diets. Plasma renin activity (PRA) and aldosterone concentration rose and fell significantly following the LS and HS diets but the sensitivity of renin response to changes in salt intake was blunted during normal pregnancy. Women who later developed PIH, when studied whilst normotensive, failed to stimulate plasma aldosterone after salt depletion in their second trimester and did not exhibit the ‘sodium-independent’ component of PRA seen in continuously normotensive subjects at this stage.

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