Endocrine Abstracts

Towards the end of pregnancy, when maternal steroidogenesis is stimulated, the fetal adrenal gland undergoes significant developmental changes. To test responsiveness to external stimuli at this stage, we fed pregnant rats with diets containing 0.03% (low), 0.3% (normal) or 3% (high) sodium to manipulate aldosterone synthesis. Dietary sodium variations had no deleterious effects on numbers or weights of foetuses at embryo day 20. Maternal adrenal weights were unaffected by diet although dietary sodium restriction increased the width and cell size of the zona glomerulosa. Fetal adrenals of high sodium mothers weighed less than those of normal diet mothers (P<0.02). Expression of maternal and fetal 11 beta-hydroxylase (CYP11B1) and aldosterone synthase (CYP11B2) were assessed by competitive RTPCR, western blotting and immunocytochemical techniques and by measuring plasma steroid concentrations. After feeding a low sodium diet, maternal expression of adrenal CYP11B2 mRNA at day 20 was approximately nine fold higher than that of tissues from rats fed a normal diet which in turn was six fold higher than that of the high sodium group (P < 0.001). Qualitatively similar changes in maternal adrenal CYP11B2 protein levels (P < 0.05) were seen although differences (two fold) were more modest. Fetal expression of adrenal CYP11B2 mRNA and protein was generally much lower than that of the maternal adrenal gland which, given the limited availability of fetal tissue, imposed technical difficulties in accurately quantifying effects of diet. Nevertheless, both immunocytochemistry and western blotting suggested that expression of aldosterone synthase was increased by low sodium diet in line with changes in plasma aldosterone (P < 0.01). CYP11B1 protein and mRNA expression in fetal and maternal adrenals and fetal plasma corticosterone levels were unaffected by diet. We conclude that fetal aldosterone synthesis is stimulated by low sodium diet but that responsiveness is more refractory than the maternal renin-angiotensin-aldosterone system.