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[Functional state of the adrenal cortex in calculous cholecystitis complicated by mechanical jaundice in elederly patients].

The functional status of the adrenal cortex in 26 elderly patients suffering from calculous cholecystitis complicated with mechanical jaundice has been studied. The activation of the glucocorticoid function and the depression of the androgenic one have been found. These changes of hormonal balance were found at all the stages of surgical treatment; they were the most pronounced in case of a severe clinical course of the disease.

Adrenal Cortex↗

Expression and regulation of the lipoprotein lipase gene in human adrenal cortex.

Lipoprotein lipase (LPL), an enzyme which hydrolyzes triglycerides and participates in the catabolism of remnant lipoproteins, plays a crucial role in energy and lipid metabolism. The goal of this study was to analyze the expression and regulation of the LPL gene in human adrenals. Reverse transcriptase-polymerase chain reaction amplification and sequence analysis demonstrated the presence of LPL mRNA in fetal and adult human adrenal cortex. Furthermore, the human adrenocortical carcinoma cell line, NCI-H295, expresses LPL mRNA and protein, which is localized to the outer cellular membrane as demonstrated by immunofluorescence confocal microscopy and can be released in the medium by heparin addition. To asses whether the LPL gene is regulated by agents regulating adrenal steroidogenesis, NCI-H295 cells were treated with activators of second messenger systems. Whereas the calcium-ionophore A23187 did not affect LPL gene expression, treatment with phorbol 12-myristate 13-acetate decreased LPL mRNA levels in a time- and dose-dependent manner. This decrease after phorbol 12-myristate 13-acetate was associated with diminished heparin-releasable LPL mass and activity in the culture medium. Addition of the cAMP analog 8-Br-cAMP to NCI-H295 cells resulted in a rapid, but transient dose-dependent induction of LPL mRNA. Treatment with the protein synthesis inhibitor cycloheximide gradually induced, whereas simultaneous addition of cAMP and cycloheximide superinduced LPL mRNA levels. Nuclear run-on analysis indicated that the effects of cAMP and cycloheximide occurred at the transcriptional and post-transcriptional level, respectively. Transient co-transfection assays demonstrated that the first 230 base pairs of the proximal LPL promoter contain a cAMP-responsive element activated by protein kinase A and transcription factors belonging to the CREB/CREM family. These data indicate that LPL is expressed in human adrenal cortex and regulated in NCI-H295 adrenocortical carcinoma cells by activators of the protein kinase A and protein kinase C second messenger pathways in a manner comparable to P450scc, which catalyzes the first step in adrenal steroidogenesis. These observations suggest a role for LPL in adrenal energy and/or lipid metabolism and possibly in steroidogenesis.

8-Bromo Cyclic Adenosine Monophosphate↗

Differential suppression of the outer and inner zones of the adrenal cortex of the guinea pig.

To examine the regulation of the zona fasciculata and the zona reticularis of the guinea pig adrenal cortex, animals were placed on a chronic regimen of dexamethasone. Changes in adrenal zonal weight, cholesterol side-chain cleavage activity, and tissue and serum steroid concentrations were measured after 1 month of dexamethasone administration. With dexamethasone treatment, the weight of the outer zone (glomerulosa/fasciculata) decreased significantly, while the weight of the inner zone (reticularis) did not change. Cholesterol side-chain cleavage activity in mitochondria isolated from the outer zone also declined significantly, while a similar activity in the inner zone did not change. The serum cortisol concentration in response to dexamethasone administration decreased by 85%, as did the concentrations of cortisol and progesterone in the outer zone; the concentration of cortisol in the inner zone decreased by only one third, while the concentration of progesterone did not change. These results in association with previous reports indicate that the zona reticularis of the guinea pig adrenal cortex (in contrast to the zona fasciculata) is not regulated by ACTH in terms of either steroidogenesis or maintenance of cell growth.

Adrenal Cortex↗

[Adrenal cortex function after local, peridural and potentiated peridural anesthesia].

The study of the adrenal function in local anesthesia and one-moment peridural anesthesia in operations for analogous affections--venous varicosity of the lower limbs, indicated no differences in changes of the adrenal cortex functioning. In one-moment peridural anesthesia, potentiated with neurolentanalgesics a tendency was observed to an increased glucocorticoid function of the adrenal gland, which should be ascribed to the effect of neuroleptanalgesics.

17-Hydroxycorticosteroids↗

Arginin-vasopressin regulates proliferative activity of the regenerating rat adrenal cortex.

Enucleation-induced adrenal regeneration is a classic model to investigate adrenocortical proliferation in vivo, which is dependent not only on pituitary ACTH release, but also on various other neural and endocrine signals. Arginin-vasopressin (AVP), mainly acting via V1 receptors, regulates hypothalamic-hypophyseal-adrenal axis function, acting on both its central and peripheral branches. Here, we studied whether endogenous AVP system modulates rat adrenal regeneration. Reverse transcription-polymerase chain reaction (PCR) detected only the mRNAs of V1a and V1b receptors in normal and regenerating adrenals. The expression was very low, and semi-quantitative conventional and real-time PCR showed that it was down-regulated in regenerating adrenals in relation to the time elapsed from enucleation. AVP (three subcutaneous injections 28, 16 and 4 h before sacrifice) raised metaphase index at day 5, but not at day 8 of regeneration. Unexpectedly, both V1-receptor and V2-receptor antagonists increased metaphase index at days 5 and 8 of regeneration. Neither AVP nor AVP-receptor antagonists affected plasma levels of corticosterone in rats bearing regenerating adrenals. It is concluded that AVP, acting via V1 receptors located in adrenals, exerts a stimulating effects on adrenal regeneration. Due to the down-regulation of V1-receptor expression in regenerating adrenals, this effect is very weak and is easily overcome by a tonic inhibitory action of endogenous AVP systems probably involving extra-adrenal indirect mechanisms.

Adrenal Cortex↗