The ontogenesis of cells containing polypeptide hormones (ACTH, MSH, LPH, GH and Prolactin) was investigated in the fetal rat hypophysis by immunohistochemistry using the peroxidase-antiperoxidase complex. Corticotrophs, melanotrophs and lipotropic cells were revealed earlier in the pars distalis than in the pars intermedia. In the pars distalis, cells producing LPH were found in the morning of day 15 of gestation using anti-gamma- or anti-beta-LPH sera, and in afternoon using anti-alpha- or beta-endorphin sera. Cells containing beta-MSH were observed from the afternoon of day 15. The cells stainable with the anti-alpha-MSH, anti-beta-(17--39)ACTH and anti-beta-(1--24)ACTH sera appeared on day 16. In the pars intermedia, the cells producing alpha-MSH, beta-MSH, alpha- and beta-endorphin, gamma- and beta-LPH were observed in the morning of day 17, while cells containing ACTH were only revealed in the afternoon of the same day of gestation. Based on the treatment of serial paraffin sections with various antisera, it was clearly shown that MSH, ACTH, and LPH occur in the same cells located in the pars distalis as in the pars intermedia. The development of the corticotrophs, melanotrophs and lipotropic cells does not require the presence of the fetal hypothalamus or other central nervous structures. The pituitary glands of 21 day-old fetus encephalectomized on day 16 showed as many reactive cells as those of the littermate controls. The somatotrophs were first revealed in the pars distalis in the afternoon of day 19. The cells producing prolactin were not observed before day 21 of gestation. On some cases GH and prolactin were found together in one cell. The cytodifferentiation of GH and prolactin cells is apparently not under hypothalamic control.

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Objective: This study aimed at determining, in the term pregnant rat, whether maternal and fetal plasma atrial natriuretic peptide (ANP) concentrations were modified in response to an oral sodium load, and to investigate whether any changes in plasma concentrations were able to modify the density and affinity of the different ANP-binding site subtypes in maternal and fetal kidneys and adrenal glands. Methods: Pregnant rats kept in metabolic cages were divided into two groups. The normal sodium diet group had free access to rat chow and tap water whereas the high sodium diet group received 1% NaCl as drinking water for 10 consecutive days from day 11 to day 21 of gestation with free access to standard rat chow. Pregnant rats from both groups were killed by decapitation on day 21 of gestation. The plasma ANP and aldosterone concentrations were determined by RIA. The density and affinity of ANP receptors were determined in the maternal and fetal adrenal glands and kidneys. Results: In the pregnant rats on the high-salt diet, the sodium and water intakes, as well as the urine volume and sodium excretion, were significantly higher than in the control group. After 10 days of high-salt intake, water and sodium retentions were not significantly different in the two groups, indicating that the pregnant rats were able to excrete excess salt. The high sodium intake did not change the body weight of the pregnant rats but did increase the body weight of the fetal rats. Maternal and fetal hematocrits remained unchanged in both groups, the high sodium intake did not modify plasma sodium concentration in the maternal rats but increased that of the fetuses, indicating an accumulation of sodium in the fetal rats. The dietary sodium intake did not change the plasma ANP concentrations but significantly decreased the plasma aldosterone concentrations in both the maternal and fetal rats. In response to the high-salt diet, the density and affinity of total ANP, ANPb and ANPc receptors were not altered in the maternal isolated renal glomeruli or the adrenal zona glomerulosa membranes or the fetal adrenal gland and kidney membrane preparations. Conclusion: These results suggest that ANP is not involved in the regulation of water and electrolyte balance in maternal and fetal rats during salt-loaded intake.

To investigate whether the hypothalamus is involved in the cytodifferentiation of the anterior pituitary gland, rat foetuses were encephalectomized in utero on day 16 of pregnancy. Pituitary sections from encephalectomized and normal littermate foetuses were studied on day 21 with the immunofluorescence technique using antibodies anti alpha-MSH, anti beta-MSH, anti alpha-(17-39) ACTH and anti beta-(1-24) ACTH. On day 16, only the anti beta-MSH revealed a few cells in the pars distalis but not in the pars intermedia. On the other hand, on day 21, the pituitary cells reacting with antibodies anti alpha-MSH, anti beta-MSH and anti alpha-(17-39) ACTH were as numerous in the encephalectomized foetuses as in the normal littermate foetuses. The cells revealed with the antibody anti beta-(1-24) ACTH were less numerous and less fluorescent in the pars distalis and intermedia of the hypophysis of the encephalectomized foetuses. On day 21, the adrenals of the encephalectomized foetuses were atrophied in comparison with those of the normal littermate foetuses but they were larger than on day 16. These data suggest that the cytodifferentiation of the corticotroph and melanotroph cells of the hypophysis occurs without the influence of the hypothalamus which is necessary for the normal release of ACTH.

The in-vitro release of ACTH by fetal rat pituitary glands on days 17, 19 and 21 of pregnancy was measured using radioimmunoassay. The spontaneous release of ACTH, expressed in pg ACTH/gland per h, increased with fetal age, in correlation with the sharp rise in pituitary ACTH content. However, since pituitary ACTH content was nearly sevenfold higher at term than on day 17, while basal release of ACTH was only threefold higher, one can speculate that the spontaneous release of ACTH was proportionally greater on day 17 than on day 21 of gestation. As corticosterone, at a physiological concentration (865 nmol/l), reduced ACTH release, it was concluded that the pituitary gland was one site of the negative feedback action of the corticosteroids during fetal life. Quantities of synthetic ovine corticotrophin releasing factor (CRF) which gave concentrations of 0.3-30 nmol/l in the incubation medium induced a sharp rise in ACTH release which was log-dose dependent between 0.3 and 3 nmolCRF /1 on day 17 and between 0.3 and 30 nmolCRF /1 on days 19 and 21. The response to CRF increased with fetal age. Quantities of arginine vasopressin (AVP) which gave concentrations of 2-200 nmol/l stimulated ACTH release at all stages of gestation investigated. However, the response to AVP was much lower than that to CRF. Potentiation of CRF-induced ACTH release was not observed when whole pituitary glands from 21-day-old fetuses were incubated with AVP (20 nmol/1) + CRF ( 3nmol /1). Such results were correlated with the ontogenesis of immunoreactive vasopressin- and CRF-containing fibres in the median eminence of the rat fetus, as well as with the CRF-like immunoreactivity present in adult rat pituitary portal plasma and the AVP content of the fetal rat hypophysis.