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PubMed1981

Failure of chronic administration of the angiotensin I-converting enzyme inhibitor, Teprotide (SQ 20881), to affect the ultrastructure of the adrenal cortex and the aldosterone secretion in the rat.

Administration of Teprotide (SQ 20881), an angiotensin I-converting enzyme inhibitor for up to 10 weeks at a dose of 3 mg. per kg., subcutaneously, twice a day in the rat, effected no change in the ultrastructure of the adrenal cortex nor in the concentration of serum aldosterone. A significant increase (p less than 0.05) in renin granulation indices which was already apparent after 3 weeks of treatment with Teprotide was even more definitive after 10 weeks (p less than 0.01). Moderate renal hypertrophy was present in rats receiving the drug for 3 weeks. Findings pertaining to aldosterone production differed from those reported following acute administration of Teprotide wherein a decrease in the production of serum aldosterone and an increase in plasma renin activity was observed. It has been suggested that decreased aldosterone production following acute administration of Teprotide is a consequence of decreased stimulus of the zona glomerulosa due to diminished synthesis of angiotensin II. If this is the case, mechanisms other than angiotensin II stimulation of the zona glomerulosa must control aldosterone synthesis, perhaps through hormones of the adrenal cortex. Another possibility could be that angiotensin II synthesis may be obtained, after an interval, through an alternative pathway.

Adrenal Cortex↗
PubMed1990

Effects of splanchnic nerve stimulation on the adrenal cortex may be mediated by chromaffin cells in a paracrine manner.

The effects of nerve activation and of the catecholamines epinephrine and norepinephrine on adrenal corticosteroid release were investigated in intact isolated perfused pig adrenals with preserved nerve supply. To study the contact zones of medullary and cortical tissues, porcine adrenals were examined on the histological and ultrastructural levels. Splanchnic nerve activation stimulated in parallel the release of epinephrine (from a basal value of 0.31 +/- 0.11 to 8.13 +/- 0.60 microgram/min) and norepinephrine (from 0.76 +/- 0.68 to 12.94 +/- 3.58 micrograms/min) and the release of the corticosteroids cortisol (from 0.62 +/- 0.19 to 2.00 +/- 0.35 micrograms/min) and aldosterone (from 3.34 +/- 0.59 to 7.53 +/- 1.63 ng sigma in). Also, perfusion of the isolated adrenals with catecholamines provoked a significant release of the corticosteroids. Epinephrine (10(-6) M) stimulated the release of cortisol (from 0.59 +/- 0.31 to 2.66 +/- 0.34 micrograms/min) and aldosterone (from 2.12 +/- 0.42 to 4.68 +/- 0.92 ng/min). Norepinephrine (10(-6) M) stimulated the release of cortisol (from 0.26 +/- 0.07 to 1.28 +/- 0.10 micrograms/min) and aldosterone (from 1.28 +/- 0.37 to 3.57 +/- 0.80 ng/min). Using an immunostaining for synaptophysin, which is specific for neuroendocrine cells, chromaffin cells could be detected within all three zones of the adrenal cortex. The two endocrine tissues appear to be closely interwoven. On the ultrastructural level, medullary cells are in apposition to cortical cells, with close cellular contacts. These results show that the release of corticosteroids cortisol and aldosterone can be stimulated through the sympatho-adrenal system. Taking into consideration the close colocalization of cortical and medullary tissues, this stimulation may be mediated by chromaffin cells in a paracrine manner.

Adrenal Cortex↗
PubMed1983

[Seasonal dynamics of cellular mitotic activity in the adenohypophysis and adrenal cortex of normal rats and under the stress reaction].

The experiments have been performed in 162 white non-inbred male rats. The animals are sacrificed on the third week of every month between 11 A. M. and 13 P. M. Some essential changes in the mitotic coefficient (MC) are noted in the organs of the hypophysis-adrenal system during 1 year. In the intact rats adenohypophysis the MC reaches its maximum in March, and in September in drops to its minimal value. In the glomerular and the fascicular-retinal zones of the intact animal adrenal cortex, two periods with an elevated mitotic activity are noted during the annual cycle (in spring and in autumn). Formalin stress produces a decrease in the adenohypophysis, and in the fascicular-retinal zone of the adrenal cortex--an increase of the MC. In the fascicular-retinal zone there is not any reaction only in May and June. Perhaps, the reason is in some seasonal changes of reactivity of the zone mentioned to ACTH. The seasonal dynamics of the MC in the hypophysis-adrenal system organs is in general maintained under the stress.

Adrenal Cortex↗
PubMed1995

Analysis of effects of corticotropin, forskolin and fluoride on activity of adenylate cyclase of bovine adrenal cortex.

A mathematical model relating the activity of adenylate cyclase (AC) with concentrations of stimulators, equilibrium dissociation constants, specific activity and efficacies of AC depending on the states of its binding sites has been developed and used for analysis of the data on activation of AC of bovine adrenal cortex plasma membranes presented in (De Foresta et al. (1987) FEBS Lett. 216, 107-112). Equilibrium dissociation constants. chi h and chi l, corresponding to high- and low-affinity forskolin-binding sites were estimated to be 0.37 and 17 microM: these constants characterize forskolin's potency more adequately than does ED50, the concentration eliciting half-asymptotic activity of AC. Corticotropin does not affect the affinity of AC for forskolin whereas fluoride increases this affinity, thus augmenting forskolin's potency. Hormone receptor of adenylate cyclase of bovine adrenal cortex has been suggested to have two or more binding sites for corticotropin. Some unidentified factor(s) may be responsible for the differences found in adenylate cyclase activity in different experiments carried out under similar conditions. The model applied for the analysis may be thought to be the best means for the moment to relate dose-response dependencies with what is known or can be hypothesized about the mechanisms underlying activation of adenylate cyclase.

Adenylyl Cyclases↗
PubMed2005

[Histological and molecular study of fetal human adrenal cortex (12-36 wk)].

Histological and functional characteristics of the fetal human adrenals was studied in 119 normal fetuses aged 12 to 36 weeks development (WD). Immunocytochemical detection of steroidogenesis enzyme (3beta-HSD and P450 c21) and evaluation of cell proliferation using two nuclear markers (Ki-67 and PCNA) were performed in 70 of them. The human fetal adrenal cortex is composed of two morphologically distinct zones: the definitive peripheral zone and the fetal inner zone. From the 12th WD, we observed expression of an adherence protein (NCAM) and two steroidogenesis enzymes (3beta-HSD and P450 c21) in the definitive zone cells, attesting to the capacity of these cells to synthesize mineralocorticoids and/or cortisol. In the fetal zone, only P450 c21 immunoreactivity was detected. From the 14th WD, a transitional zone between the definitive zone and the fetal zone was identified by immunocytochemistry, with expression of 3b-HSD from the 21st WD. Only cells of the definitive zone proliferated from the 12th to 25th WD. The indexes of proliferation of PCNA and Ki-67, 40% and 25% respectively, decreased gradually and were lower than 1% at the 25th WD.

3-Hydroxysteroid Dehydrogenases↗
PubMed1982

Cumene hydroperoxide supported demethylation of N,N-dimethylaniline by cytochrome P-450 from adrenal cortex mitochondria.

The interaction of highly purified cytochrome P-450 from bovine adrenal cortex mitochondria (cytochrome P-450scc) with N,N-dimethylaniline (DMA), aniline, N-dimethylcyclohexylamine and cumene hydroperoxide (CHP) has been investigated. The formation of complexes between cytochrome P-450scc and the above listed compounds could be demonstrated. The reaction of oxidative demethylation of DMA by cumene hydroperoxide involving cytochrome P-450scc has been carried out at 37 degrees C; the mechanism of this process is discussed. Incubation of cytochrome P-450scc with negatively charged phospholipids, phosphatidylglycerol (PG), and phosphatidylinosite (PI) exerts an inhibiting effect on the reaction of oxidative demethylation. The interaction of cytochrome P-450scc with CHP is accompanied by hemoprotein destruction in a complex biphasic way. The process of oxidative demethylation of DMA in the system of cytochrome P-450scc-CHP has been concluded to have a predominantly radical character.

Adrenal Cortex↗
PubMed1975

[Biosynthetis in vitro of estrogens by an adrenal cortex tumor].

A polysecretory cortico-adrenal tumor from a 46 year old woman was incubated in presence of tritiated pregnenolone and progesterone. Nine estrogens were isolated and identified by radio-gas-chromatography. This outstanding synthesis ability was in line with the high rates of urinary estrogens found in this patient.

Adrenal Cortex Neoplasms↗
PubMed1980

Growth and cytodifferentiation of the fetal lamb adrenal cortex prior to parturition.

Growth patterns and cytodifferentiation of the fetal lamb adrenal cortex, from 136 days of gestation to birth at normal term, have been examined. The gland almost doubles in weight over this period (0.45--0.80 g) and the inner cortical zone (zona fasciculata+zona reticularis) nearly quadruples in thickness (0.33--1.25 mm). The phase of rapid growth has begun by 136 days, and the growth patterns are essentially linear. The inner cortical zone consists of light and dark cells, the former increasing in number proportionately more than the dark cells. This change in the cell ratio is linked with increased fetal production of cortisol. As growth and differentiation proceed the light cells increasingly possess a more vesicular SER; mitochondria of the orthodox configuration, with predominantly vesicular cristae; a well developed Golgi complex with numerous small, bristle coated vesicles; and dark granules near the Golgi complex, in the peripheral cytoplasm, and external to the cells. The sixfold increase in the volume of the inner cortical zone and the ultrastructural evidence of cytodifferentiation appear adequate to account for the known increase in the fetal synthesis of cortisol during this stage of pregnancy.

Adrenal Cortex↗
PubMed1987

Alpha-inhibin gene expression occurs in the ovine adrenal cortex, and is regulated by adrenocorticotropin.

Inhibin is a glycoprotein hormone composed of two nonidentical subunits. It is produced by the ovary and testis and plays a vital role in gonadal function by inhibiting the secretion of FSH. More recently, additional activities associated with inhibin peptides have been identified. Inhibin heterodimers (alpha-beta) are reported to act directly on ovarian granulosa cells and inhibit estrogen production induced by FSH. Furthermore, homodimers of beta-inhibin subunits stimulate the secretion of FSH, an activity that is directly opposite to that of inhibin. Each of these inhibin-related activities are concerned with the hypothalamic-pituitary-gonadal axis. We have investigated further the complexity of inhibin activity by determining whether inhibin genes are expressed in nongonadal tissue. RNA hybridization experiments demonstrate that the alpha-inhibin gene is expressed in the sheep adrenal cortex and hybridization histochemistry shows that this gene is expressed in each of the functional zones within the cortex. Dot blot analysis showed that the level of alpha mRNA within the adrenal is influenced by ACTH, one of the major regulators of adrenal cortex function. These observations imply that there are inhibin-related peptides not directly associated with the gonads. beta-inhibin gene expression was not clearly detected in the adrenal and we conclude that if expression occurs then it does so at extremely low levels.

Adrenal Cortex↗
PubMed1995

Action of opioid peptides on the rat adrenal cortex: stimulation of steroid secretion through a specific mu opioid receptor.

While there have been several studies on the actions of opioid peptides on adrenocortical steroidogenesis, the results of these studies have failed to resolve the question as to whether these peptides exert a direct action on the adrenal cortex. The present studies were designed to address this question directly, using collagenase-dispersed rat zona glomerulosa and zonae fasciculata/reticularis cells incubated in vitro. The results obtained clearly show that the opioid peptides tested (beta-endorphin, Leu-enkephalin, Met-enkephalin, and its long-acting analogue, DALA) all exerted a significant stimulatory effect on aldosterone secretion by zona glomerulosa cells and all, except Leu-enkephalin, stimulated corticosterone secretion by inner zone cells. The response was shown to be inhibited by naloxone. There did not appear to be a significant interaction between the effects of ACTH and the opioid peptides on adrenocortical cells. Studies using specific agonists for opioid receptor subtypes (DAMGO, DPDPE and U-50488H, specific for mu, delta and kappa receptors respectively) showed that the effect of opioid peptides on the zona glomerulosa appeared to be mediated exclusively by mu receptors while the response of inner zone cells was mediated by both mu and, to a lesser extent, kappa receptors. Finally, studies on the second messenger systems activated by the opioid peptides and the receptor agonists showed that these peptides act to increase labelling of inositol trisphosphate, and strongly suggest that, in the rat adrenal cortex, both mu and kappa opioid receptors are linked to the activation of phospholipase C.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1983

Changes in blood cortisol and aldosterone levels and ultrastructure of the adrenal cortex during hemorrhagic shock.

Changes of secretory activity and structure of the adrenal cortex were observed in dogs subjected to hemorrhagic shock. Blood cortisol and aldosterone levels were rapidly increased after hemorrhage. The cortisol level reached a maximum value about 5 times that of normal 1 h after hemorrhage, while aldosterone levels attained maximum levels showing a 10-fold increase over normal, considerably later (at the end of the impending stage) than the cortisol. Cortisol secretion was quickly depleted at the end of critical stage and terminal stage of normovolemic shock, while the aldosterone secretion remained relatively high. Morphologically, sticking of leukocytes to the sinusoidal wall and accumulation of SER around lipid droplets in the fasciculata and reticularis cells became conspicuous 1 h after hemorrhage. At the end of the impending stage, infiltration of leukocytes occurred in the zona fasciculata and reticularis. Irregular masses of fibrin strands appeared in the sinusoidal space and at large gaps of the sinusoidal wall. Degenerative changes such as aggregation of SER, dilatation of endoplasmic reticulum and edema were observed in the cells of zona fasciculata and reticularis, especially of inner half of the former. At the end of the critical stage, small necrotic foci and hemorrhage with inflammatory infiltration were scattered in the inner half of the zona fasciculata. Degeneration of the cells of zona fasciculata and reticularis became more severe in this period, while the cells of zona glomerulosa remained unchanged. At the terminal stage of normovolemic shock after reinfusion, degeneration and necrosis were remarkable in the cells of zona fasciculata and reticularis, especially of the inner half of the zona fasciculata. Moreover, destruction of cordal structure, hemorrhage and inflammatory infiltration were distinct in the zona fasciculata and reticularis, while the zona glomerulosa was relatively well preserved.

Adrenal Cortex↗
PubMed1976

Pigmented adenoma of adrenal cortex associated with Cushing's syndrome: light and electron microscopic study.

A pigmented adenoma of the adrenal cortex was surgically removed from a thirty-nine-year-old woman with clinical and biochemical manifestations of Cushing's syndrome. Light and electron microscopic study revealed numerous pigment granules, exhibiting the structural features of lipofuscin in the cytoplasm of the adenoma cells. It appears that adrenocortical adenomas with excessive pigment deposition can be accompanied by increased production of corticosteroid hormones.

Adenoma↗