Advertisement
Research Article Free access | 10.1172/JCI107274
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06510
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510
Find articles by Zusman, R. in: JCI | PubMed | Google Scholar
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06510
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510
Find articles by Spector, D. in: JCI | PubMed | Google Scholar
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06510
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510
Find articles by Caldwell, B. in: JCI | PubMed | Google Scholar
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06510
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510
Find articles by Speroff, L. in: JCI | PubMed | Google Scholar
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06510
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510
Find articles by Schneider, G. in: JCI | PubMed | Google Scholar
Department of Obstetrics and Gynecology, Yale University School of Medicine, New Haven, Connecticut 06510
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510
Find articles by Mulrow, P. in: JCI | PubMed | Google Scholar
Published May 1, 1973 - More info
It has been suggested that prostaglandins may be involved in the control of sodium homeostasis. Prostaglandin A and prostaglandin E have been shown to increase renal blood flow and urinary sodium excretion and prostaglandin A has been shown to stimulate aldosterone release. The purpose of this study was to determine the effect of chronic sodium loading and sodium restriction on plasma prostaglandin A, E, and F concentrations.
Seven normal human volunteers were placed on three sodium intake diets: (a) ad lib. sodium intake, (b) high sodium intake, and (c) low sodium intake. Plasma prostaglandin A, E, and F concentrations were measured by radioimmunoassay.
Mean prostaglandin A levels on the ad lib. diet were 1.60 ng/ml. Prostaglandin A levels decreased 49% to 0.82 ng/ml on the high sodium intake and increased 34% to 2.14 ng/ml on the low sodium intake. Prostaglandin A levels increased 161% on the low sodium diet in comparison with levels on the high sodium diet. Plasma prostaglandin E and F concentrations did not change significantly during variation in sodium intake.
These results show that dietary sodium content markedly effects plasma prostaglandin A levels and that prostaglandins may play a role in the physiologic mechanism of sodium homeostasis.