Compensatory adrenal growth: a neurally mediated reflex

Mf, Dallman; Engeland, William C.; Shinsako, Jeanette

doi:10.1152/ajplegacy.1976.231.2.408

Cited by 92 publications

(37 citation statements)

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“…The procedure in which one adrenal is surgically removed results in a rapid increase (within 24 h) in the size of the contralateral gland as measured by an increase in wet weight, and DNA and RNA synthesis. The mechanisms that regulate the process have been investigated extensively, and it has been demonstrated that a neural circuit exists involving the hypothalamus which when stimulated by manipulation of one adrenal stimulates growth of the other gland (Dallman et al 1976(Dallman et al , 1980. Despite the neural involvement, there is a still a requirement for the pituitary because, although compensatory growth does occur in hypophysectomised animals, it is against the background of a gland undergoing rapid adrenal atrophy and appears more of a slowing of this atrophy rather than any increase in size (Dallman et al 1980).…”

Section: Compensatory Adrenal Growthmentioning

confidence: 99%

60 YEARS OF POMC: N-terminal POMC peptides and adrenal growth

Bicknell

2016

Journal of Molecular Endocrinology

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The peptide hormones contained within the sequence of proopiomelanocortin (POMC) have diverse roles ranging from pigmentation to regulation of adrenal function to control of our appetite. It is generally acknowledged to be the archetypal hormone precursor, and as its biology has been unravelled, so too have many of the basic principles of hormone biosynthesis and processing. This short review focuses on one group of its peptide products, namely, those derived from the N-terminal of POMC and their role in the regulation of adrenal growth. From a historical and a personal perspective, it describes how their role in regulating proliferation of the adrenal cortex was identified and also highlights the key questions that remain to be answered.

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Section: Compensatory Adrenal Growthmentioning

confidence: 99%

60 YEARS OF POMC: N-terminal POMC peptides and adrenal growth

Bicknell

2016

Journal of Molecular Endocrinology

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“…Dallman (16) distinguishes four types of adrenal cortex growth and each of them is differentially regulated. Enucleation-induced adrenocortical regeneration resembles growth of the gland at early embryogenesis and depends on several neural and endocrine signals (17)(18)(19)(20)(21), while unilateral adrenalectomy-induced compensatory growth is primarily neurally mediated (16,(22)(23)(24)(25). Adrenocortical growth related to maturation is probably regulated by numerous growth factors while adrenocorticotropic hormone (ACTH)-induced growth primarily depends on adrenocortical cell proliferation (16,26).…”

Section: Introductionmentioning

confidence: 99%

Neuromedin U enhances proliferation of ACTH-stimulated adrenocortical cells in the rat

Trejter

Guidolin²,

Nowak³

et al. 1998

Int J Mol Med

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Abstract. Neuromedin U (NMU) is a brain-gut peptide involved in the regulation of the hypothalamic-pituitaryadrenal axis and adrenocortical cell proliferation. In this study, we investigated the effects of NMU8 (three subcutaneous injections of 6.0 nmol/100 g, 24, 16 and 8 h before autopsy) on the adrenal glands of rats treated for 2 or 4 days with a low (2 μg/100 g body weight/24 h) or a high (8 μg) dose of adrenocorticotropic hormone (ACTH). As revealed by RT-PCR, ACTH treatment did not prevent expression of NMUR1 in rat adrenal cortex. At day 4 of ACTH administration, the weight of adrenals was lower than at day 2. NMU8 administration prevented ACTH-induced increases of adrenal weight at day 2 of the experiment. ACTH plasma concentrations were increased in all ACTH-administered rats. NMU8 administration increased ACTH plasma concentration at day 2 of the lower ACTH dose-treated group while it reduced the ACTH plasma level at day 4 in the higher ACTH dose-administered rats. In all groups of ACTH-treated rats, NMU8 changed neither aldosterone nor corticosterone plasma concentrations. In the zona glomerulosa (ZG), NMU8 increased metaphase index at days 2 and 4 in the lower ACTH dose-treated group and had no statistically significant effect in rats treated with the higher ACTH dose. In the zona fasciculata (ZF), NMU8 administration increased metaphase index at day 2 in the lower ACTH dose-treated group but reduced metaphase index at day 4 in the higher dose ACTHadministered rats. NMU8 reduced the number of cells per unit area both in ZG and ZF at day 2 in the higher ACTH dose-treated rats. In the remaining groups NMU8 did not produce statistically significant changes in the number of cells per unit area. Thus, our findings demonstrate that exogenous NMU may stimulate proliferation primarily of the cortical ZG cells in rats administered with ACTH, although at high doses of exogenous corticotropin an opposite effect occurred.

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“…21 and 22). Also, neural inputs seem to mediate compensatory growth in the remaining adrenal after unilateral adrenalectomy (23). The sympathoadrenomedullary system produces these effects on the adrenal cortex in part by increasing sensitivity to ACTH.…”

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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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Compensatory adrenal growth: a neurally mediated reflex

Cited by 92 publications

References 0 publications

60 YEARS OF POMC: N-terminal POMC peptides and adrenal growth

60 YEARS OF POMC: N-terminal POMC peptides and adrenal growth

Neuromedin U enhances proliferation of ACTH-stimulated adrenocortical cells in the rat

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

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