PubMed · 14849536
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F E KRUSIUS. 1951. [Adrenal cortex function tests].. https://pubmed.ncbi.nlm.nih.gov/14849536/
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To understand the effects of polychlorinated biphenyls (PCBs) on adrenal aldosterone biosynthesis, we have performed a systematical study to characterize the corresponding steroidogenic response of human adrenocortical cell line H295R to PCB126 exposure. We found that PCB126 at high concentrations stimulated basal and inducible aldosterone production. The aldosterone induction occurred concomitantly with activation of the CYP11B2 gene. Despite the fact that PCB126 acted in synergy with both potassium and angiotensin II (Ang II) in activation of aldosterone synthesis, PCB126 only modestly increased CYP11B2 mRNA expression in the presence of Ang II contrary to the synergistic transcriptional induction elicited by PCB126 and potassium. This implicated that PCB126 had differential interactions with the potassium and Ang II signaling systems in the regulation of aldosterone biosynthesis. In addition, high concentrations of PCB126 elevated transcriptional expression of the type I Ang II receptor (AT(1)) and might thus sensitize the cellular Ang II responsiveness in both basal and inducible aldosterone biosynthesis. SF-1 was not involved in the PCB126-induced transcriptional regulation despite its importance in steroidogenic gene activation.
We previously demonstrated decreased adrenal content of a mitochondrial cholesterol transporter [peripheral-type benzodiazepine receptor (PBR)] during the first postnatal week in rats, when ACTH-inducible steroidogenesis is low. Here we report that the expression of PBR protein and mRNA increases throughout the neonatal/juvenile period in rats in parallel with ACTH-inducible steroidogenesis in vitro. We also previously reported that chronic stimulation of rat pups with daily ACTH injections augmented the steroidogenic response of the developing adrenal cortex. We therefore tested the hypotheses that the change in phenotype induced by ACTH was permanent, and that the effects of ACTH were mediated by increased PBR expression. Pups were injected with ACTH or saline from postnatal d (pd) 2-8 or 2-14. Another group of pups received ACTH from pd 2-7, followed by saline from pd 8-14. On the final day, all pups were challenged with a test injection of ACTH or saline. Exposure to ACTH, but not saline, for 1 wk significantly increased adrenal mass, the corticosterone response to ACTH, and the expression of PBR protein and mRNA. Continued ACTH treatment for a second week maintained adrenal mass, steroidogenesis, and PBR mRNA expression. When ACTH was withdrawn after 1 wk and replaced with daily saline injections, however, adrenal mass, ACTH-inducible steroidogenesis, and PBR expression returned to levels comparable to those in age-matched saline controls (i.e. animals that had not received ACTH injections during the first 2 wk). Thus, although ACTH was capable of inducing increased steroidogenic capacity of the juvenile rat adrenal, its effects were only manifest when pups were exposed regularly to high plasma ACTH levels. ACTH, therefore, has significant, but reversible, effects on the development of adrenocortical function, possibly mediated in part by increased expression of PBR.
Although adrenocorticotropic hormone is generally considered to play a major role in the regulation of adrenal glucocorticoid secretion, several reports have suggested that other pituitary hormones (e.g., prolactin) also play a significant role in the regulation of adrenal function. The aim of the present study was to measure the adrenocortical cell area and to determine the effects of the transition from the prepubertal to the postpubertal period on the hyperprolactinemic state induced by domperidone (4.0 mg kg-1 day-1, sc). In hyperprolactinemic adult and young rats, the adrenals were heavier, as determined at necropsy, than in the respective controls: adults (30 days: 0.16 +/- 0.008 and 0.11 +/- 0.007; 46 days: 0.17 +/- 0.006 and 0.12 +/- 0.008, and 61 days: 0.17 +/- 0.008 and 0.10 +/- 0.004 mg for treated and control animals, respectively; P < 0.05), and young rats (30 days: 0.19 +/- 0.003 and 0.16 +/- 0.007, and 60 days: 0.16 +/- 0.006 and 0.13 +/- 0.009 mg; P < 0.05). We selected randomly a circular area in which we counted the nuclei of adrenocortical cells. The area of zona fasciculata cells was increased in hyperprolactinemic adult and young rats compared to controls: adults: (61 days: 524.90 +/- 47.85 and 244.84 +/- 9.03 microm2 for treated and control animals, respectively; P < 0.05), and young rats: (15 days: 462.30 +/- 16.24 and 414.28 +/- 18.19; 60 days: 640.51 +/- 12.91 and 480.24 +/- 22.79 microm2 ; P < 0.05). Based on these data we conclude that the increase in adrenal weight observed in the hyperprolactinemic animals may be due to prolactin-induced adrenocortical cell hypertrophy.