Acute stress effects on the adrenal cortex in the rat. A biochemical and immunohistochemical study.

Pignatelli, Duarte; P, Pinto da Silva; Azevedo, M. Eugenia; Magalhães, M.M.; Magalhães, M. C.

doi:10.1080/07435809609043730

Cited by 12 publications

(8 citation statements)

References 31 publications

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“…However response to physical stressors was higher [12,16]. Our results are in line with the well established fact that ACTH and CORT levels represents the measure of the stress response intensity, particularly in its acute phase [17,18].…”

Section: Discussionsupporting

confidence: 86%

Effect of acute heat stress on rat adrenal cortex — a morphological and ultrastructural study

Petrovic-Kosanovic¹,

Veličković²,

Koko³

et al. 2012

Open Life Sciences

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The stereological structure of rat adrenal gland was analysed by light and electron microscopy after an acute (60 min) exposure to high ambient temperature (38°C). Under these conditions a significant increase in plasma corticotrophin (ACTH), serum corticosterone and aldosterone levels were observed. Histological and stereological investigation at light microscopy showed significant decrease in volume density of capsule and zona glomerulosa, increase in volume of fasciculata cells, and decrease of numerical density of zona fasciculata cells and mean diameter of blood vessels. At the ultrastructural level, volume density of nuclei and mitochondria of zona glomerulosa cells were significantly increased and that of lipid droplets decreased. Volume density of mitochondria of fasciculata cells was significantly increased, while number of lipid droplets per µm2 of cell was reduced. In the cells of zona reticularis significant increase in the number of lipid droplets was found. The response of zona glomerulosa may be interpreted as immediate reaction to dehydration, while alterations detected in zona fasciculata, which were less extensive, were related to purely stressogenic effects of high ambiental temperature.

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Section: Discussionsupporting

confidence: 86%

Effect of acute heat stress on rat adrenal cortex — a morphological and ultrastructural study

Petrovic-Kosanovic¹,

Veličković²,

Koko³

et al. 2012

Open Life Sciences

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“…The latter is particularly striking, because, contrary to what is generally believed, ACTH blocks adrenocortical cell division and reduces cell size when applied to isolated adrenal cells (85). Interestingly, it was recently recognized that corticosterone secretion had a peak preceding the elevation of ACTH induced by immobilization stress (86). As the sympathetic nervous system responds earlier than the HPA axis to stressors, it is possible that the phase advance of the corticosterone response over that of ACTH is explained by an earlier splanchnic nerve stimulation of the adrenal cortex.…”

Section: Does the Extrapituitary-adrenocortical Stress Response Constmentioning

confidence: 99%

Adrenocorticotropin (ACTH)- and Non-ACTH-Mediated Regulation of the Adrenal Cortex: Neural and Immune Inputs

Bornstein

Chrousos

1999

The Journal of Clinical Endocrinology & Metabolism

276

121

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The maintenance of life depends on the capacity of the body to sustain its steady state or homeostasis; hence, the survival of the organism relies on its ability to react and adapt to the constant bombardment by physical and emotional threats or stressors (1, 2). To accomplish this, all living beings have developed an efficient but complex adaptive response system that allows the integration of the necessary defense mechanisms directed against both external and internal stressors. This coordinated response, the stress response, involves the nervous, endocrine, and immune systems. A qualitatively and quantitatively appropriate and time-limited stress response is a prerequisite for a healthy life. Inappropriate or inappropriately excessive and chronic hyperactivation of the stress system may lead to disease and, eventually, premature death.The two major peripheral limbs of the stress system are the hypothalamic-pituitary-adrenal (HPA) axis and the sympathetic nervous system (1, 2). Their central components are, respectively, located in the hypothalamus and the brain stem. Stress-induced activation of the HPA axis is associated with release of hypothalamic CRH and vasopressin (AVP), the principal regulators of anterior pituitary corticotropin (ACTH) secretion, into the hypophyseal portal system. These hormones synergistically stimulate systemic ACTH secretion, which, in turn, stimulates the adrenal cortexes to secrete glucocorticoids. Central activation of the sympathetic neurons leads to activation of both the systemic sympathetic nervous system and, through the splanchnic nerves, the adrenal medullae (3). As the proper functioning of both the HPA axis and the sympathetic nervous system is crucial for survival and maintenance of health, it is not surprising that their regulation is developmentally plastic and complex, multilevel, and redundant. The regulation and central interaction of the HPA axis and the sympathetic nervous system and the immune system have been extensively studied and summarized in recent review articles (1, 3-5). The purpose of this brief review is to outline and discuss recent advances in the interactions and regulation of the adjacent peripheral limbs of the stress system, particularly the adrenal cortex and medulla, and to point out their implications for clinical endocrinology (Fig. 1).The adrenal gland has an astonishing capacity to adapt to various forms of acute and chronic stress (6 -8). After central activation of the HPA axis, ACTH triggers a physiologic, molecular, and morphological response of the adrenal cortex. This leads not only to glucocorticoid release, but also to up-regulation of steroidogenic cytochrome P 450 messenger ribonucleic acids (9, 10) and to conspicuous structural changes in the adrenal gland characterized by both hypervascularization and cellular hypertrophy and hyperplasia (11,12). These morphological changes are mirrored on the ultrastructural level; adrenocortical cells increase the number of their mitochondria, whereas their inner membranes form a dense vesi...

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“…However, many clinical and experimental situations have brought evidence to light that there is dissociation between plasma ACTH concentrations and cortisol secretion (3,4). Interestingly, one study showed corticosterone secretion to peak before the elevation of ACTH induced by immobilization stress (5), and that rat pups exposed to hypoxia exhibit ACTH-independent increased corticosterone release (6). Because the sympathetic nervous system responds earlier than the hypothalamus-pituitary-adrenal axis to stressors, corticosterone release before that of ACTH action may be due to earlier stimulation of the adrenal cortex via the splanchnic nerve, possibly also through NO release.…”

mentioning

confidence: 99%

The rapid release of corticosterone from the adrenal induced by ACTH is mediated by nitric oxide acting by prostaglandin E ₂

Mohn

Fernández‐Solari

Laurentiis

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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The adrenal cortex is a major stress organ in mammals that reacts rapidly to a multitude of external and internal stressors. Adrenocorticotropin (ACTH) is the main stimulator of the adrenal cortex, activating corticosteroid synthesis and secretion. We evaluated the mechanism of action of ACTH on adrenals of male rats, preserving the architecture of the gland in vitro. We demonstrated that both sodium nitroprusside (NP), a nitric oxide (NO) donor, and ACTH stimulate corticosterone release. NO mediated the acute response to ACTH because N-nitro-L-arginine methyl ester, a NO synthase inhibitor, and hemoglobin, a NO scavenger, blocked the stimulation of corticosterone release induced by ACTH. NP stimulated prostaglandin E release, which in turn stimulated corticosterone release from the adrenal. Additionally, indomethacin, which inhibits cyclooxygenase, and thereby, prostaglandin release, prevented corticosterone release from the adrenal induced by both NP and ACTH, demonstrating that prostaglandins mediate acute corticosterone release. Corticosterone content in adrenals after incubation with ACTH or NP was lower than in control glands, indicating that any de novo synthesis of corticosterone during this period was not sufficient to keep up with the release of the stored hormone. The release induced by ACTH or NP depleted the corticosterone content in the adrenal by Ϸ40% compared with the content of glands incubated in buffer. The mechanism of rapid release is as follows: NO produced by NO synthase activation by ACTH activates cyclooxygenase, which generates PGE 2, which in turn releases corticosterone stored in microvesicles and other organelles.cyclooxygenase ͉ indomethacin ͉ nitric oxide synthase ͉ N-nitro-L-arginine methyl ester

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Acute stress effects on the adrenal cortex in the rat. A biochemical and immunohistochemical study.

Cited by 12 publications

References 31 publications

Effect of acute heat stress on rat adrenal cortex — a morphological and ultrastructural study

Effect of acute heat stress on rat adrenal cortex — a morphological and ultrastructural study

Adrenocorticotropin (ACTH)- and Non-ACTH-Mediated Regulation of the Adrenal Cortex: Neural and Immune Inputs

The rapid release of corticosterone from the adrenal induced by ACTH is mediated by nitric oxide acting by prostaglandin E ₂

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Acute stress effects on the adrenal cortex in the rat. A biochemical and immunohistochemical study.

Cited by 12 publications

References 31 publications

Effect of acute heat stress on rat adrenal cortex — a morphological and ultrastructural study

Effect of acute heat stress on rat adrenal cortex — a morphological and ultrastructural study

Adrenocorticotropin (ACTH)- and Non-ACTH-Mediated Regulation of the Adrenal Cortex: Neural and Immune Inputs

The rapid release of corticosterone from the adrenal induced by ACTH is mediated by nitric oxide acting by prostaglandin E 2

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The rapid release of corticosterone from the adrenal induced by ACTH is mediated by nitric oxide acting by prostaglandin E ₂