Abstract

We read with interest the recent article of Roy-Clavel et al (Roy-Clavel E, Picard S, St-Louis J, Brochu M. Induction of intrauterine growth restriction with a low-sodium diet fed to pregnant rats. Am J Obstet Gynecol 1999;180:608-13), who reported a significantly lower birth weight among pregnant rats fed a low-sodium diet. No reference was made, however, to similar studies in human pregnancy. We studied the effects of chronic dietary sodium restriction (after organogenesis) in human pregnancy in the prevention of pregnancy-induced hypertension.1Steegers EA van Lakwijk HP Jongsma HW Fast JH de Boo T Eskes TK et al.(Patho)physiological implications of dietary sodium restriction during pregnancy: a longitudinal prospective randomised study.Br J Obstet Gynaecol. 1991; 98: 980-987Crossref PubMed Scopus (40) Google Scholar, 2van Buul BJ Steegers EA van der Maten GD Delemarre FM Jongsma HW Oosterbaan HP et al.Dietary sodium restriction does not prevent gestational hypertension: a Dutch two-center randomized trial.Hypertens Pregnancy. 1997; 16: 335-346Crossref Scopus (19) Google Scholar Healthy nulliparous women were randomly assigned at 14 weeks' gestation to either a low-sodium (20 mmol/d) dietary regimen or an unrestricted sodium intake. Compliance with the regimen was checked by measurement of 24-hour urinary sodium/creatinine ratio at monthly intervals (mean values, 6-8 mmol/mmol in the sodium-restricted group between 20 weeks' gestation and delivery vs 12 mmol/mmol in the unrestricted diet group). Like Roy-Clavel et al, we found that sodium restriction resulted in activation of the renin-aldosterone system, a decrease in plasma volume, and an increase in peripheral vascular resistance without influencing blood pressure. Maternal weight gain was lower, and dietary analysis revealed a lower intake of nutrients as well. In contrast to Roy-Clavel et al, we found no significant differences in birth or placental weight as a result of long-term dietary sodium restriction, nor did we find any significant effect on plasma concentrations of sodium, potassium, and magnesium. It is possible, however, that optimal compliance with the diet would have resulted in more pathophysiologic effects during human pregnancy as well. We found a tendency toward dysmaturity (defined as <10th percentile birth weight) in the sodium-restricted group, although the difference was not significant (relative risk, 1.48; 95% confidence interval, 0.72-3.02). Significantly higher resistance indexes of the umbilical artery in the low-sodium group3Delemarre FMC van Leest LATM Jongsma HW Steegers EAP. The effect of a low sodium diet on the uteroplacental circulation.J Matern Fetal Med. 2000; (In press)PubMed Google Scholar support the hypothesis that maternal hypovolemia as a result of this dietary intervention may influence uteroplacental perfusion. We agree that this model is of great interest for the study of vascular reactivity during pregnancy. In our opinion, however, a low mean arterial pressure does not indicate that the physiologic blunted vasopressor response in pregnancy is unaffected by a low-sodium diet. Sodium restriction decreases the responsiveness to angiotensin, probably through change in avidity of vascular angiotensin receptors.4Jaspers WJ de Jong PA Mulder AW. Decrease of angiotensin sensitivity after bed rest and strongly sodium-restricted diet.Am J Obstet Gynecol. 1983; 145: 792-796PubMed Scopus (18) Google Scholar

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