Actions of Corticotropin on the Adrenal Cortex: Biochemistry and Cell Biology

Hall, Peter F.

doi:10.1002/cphy.cp070404

Cited by 5 publications

(6 citation statements)

References 95 publications

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“…However some of these including, CGRP, SP and PACAP are primarily localized in sensory nerve fibers that do not appear to contribute to splanchnic nerve modulation of steroid production (Ulrich-Lai et al, 2006). One mechanism by which neurotransmitters can affect steroid synthesis is by induction of intracellular cyclic adenosine monophosphate (cAMP) that upregulates the rate-limiting step, the availability of free cholesterol necessary to synthesis steroids (Hall, 2001). Adrenal cAMP levels express a diurnal rhythm that is maintained in hypophysectomized animals (Guillemant et al, 1980) but reduced following splanchnic nerve transection (Ulrich-Lai et al, 2006) suggesting sympathetic responses may regulate steroid synthesis via modulating cAMP levels and the availability of free cholesterol.…”

Section: Discussionmentioning

confidence: 99%

Sympathetic nervous system contributes to enhanced corticosterone levels following chronic stress

Lowrance

Ionadi

McKay

et al. 2016

Psychoneuroendocrinology

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Exposure to chronic stress often elevates basal circulating glucocorticoids during the circadian nadir and leads to exaggerated glucocorticoid production following exposure to subsequent stressors. While glucocorticoid production is primarily mediated by the hypothalamic–pituitary–adrenal (HPA) axis, there is evidence that the sympathetic nervous system can affect diurnal glucocorticoid production by direct actions at the adrenal gland. Experiments here were designed to examine the role of the HPA and sympathetic nervous system in enhancing corticosterone production following chronic stress. Rats were exposed to a four-day stress paradigm or control conditions then exposed to acute restraint stress on the fifth day to examine corticosterone and ACTH responses. Repeated stressor exposure resulted in a small increase in corticosterone, but not ACTH, during the circadian nadir, and also resulted in exaggerated corticosterone production 5, 10, and 20 min following restraint stress. While circulating ACTH levels increased after 5 min of restraint, levels were not greater in chronic stress animals compared to controls until following 20 min. Administration of astressin (a CRH antagonist) prior to restraint stress significantly reduced ACTH responses but did not prevent the sensitized corticosterone response in chronic stress animals. In contrast, administration of chlorisondamine (a ganglionic blocker) returned basal corticosterone levels in chronic stress animals to normal levels and reduced early corticosterone production following restraint (up to 10 min) but did not block the exaggerated corticosterone response in chronic stress animals at 20 min. These data indicate that increased sympathetic nervous system tone contributes to elevated basal and rapid glucocorticoid production following chronic stress, but HPA responses likely mediate peak corticosterone responses to stressors of longer duration.

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Section: Discussionmentioning

confidence: 99%

Sympathetic nervous system contributes to enhanced corticosterone levels following chronic stress

Lowrance

Ionadi

McKay

et al. 2016

Psychoneuroendocrinology

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“…It has previously been shown that there is a diurnal rhythm in adrenal cAMP levels that persists in hypophysectomized rats (11,12); cAMP (via activation of protein kinase A) increases the amount of free cholesterol and its transfer into the mitochondria, which is considered the rate-limiting step in steroidogenesis (reviewed in Ref. 13). The present studies demonstrate that there is also a diurnal rhythm in adrenal StAR, but not adrenal PBR; StAR and PBR are two additional molecules implicated in the transport of cholesterol into the mitochondria.…”

Section: Discussionmentioning

confidence: 99%

“…Steroidogenic acute regulatory protein (StAR) and peripheral benzodiazepine receptor (PBR) are two molecules implicated in the cholesterol transport process (reviewed in Ref. 13).…”

mentioning

confidence: 99%

Adrenal splanchnic innervation contributes to the diurnal rhythm of plasma corticosterone in rats by modulating adrenal sensitivity to ACTH

Ulrich‐Lai

Arnhold

Engeland³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

195

135

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Activity of the hypothalamic-pituitary-adrenal axis is characterized by a diurnal rhythm with an AM nadir and PM peak. Splanchnic nerve transection disrupts the diurnal rhythm in plasma corticosterone; however, there is a controversy as to whether the nerve-mediated effect is 1) via inhibition in the AM vs. excitation in the PM, or 2) involves changes in adrenal sensitivity to ACTH. The present studies were designed to address these issues. Adult male rats were anesthetized and underwent bilateral transection of the thoracic splanchnic nerve or sham transection. One week after surgery, rats were killed in the AM or PM with collection of nonstress plasma for measurement of corticosterone and ACTH. Plasma corticosterone was increased in the PM relative to the AM; however, plasma corticosterone in the PM was attenuated by splanchnic nerve transection, without affecting plasma ACTH. This decrease in PM plasma corticosterone after nerve-transection was 1) associated with decreased adrenal responsivity to ACTH, 2) associated with decreased adrenal cAMP content, 3) prevented by adrenal demedullation, and 4) not affected by removal of adrenal capsaicin-sensitive afferent fibers. Repeated serial blood sampling from individual rats confirmed the excitatory effect of splanchnic innervation in the PM. These results support the hypothesis that the adrenal splanchnic innervation modulates the diurnal rhythm in plasma corticosterone by increasing adrenal responsivity to ACTH and augmenting steroidogenesis in the PM and suggest that alterations in adrenal corticosterone secretion obscured by pulsatile secretion are more clearly revealed with repeated serial blood sampling.

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“…Together, CRH and AVP act synergistically to stimulate the secretion of adrenocorticotropic hormone (ACTH) from the anterior pituitary (Antoni, 1986). Plasma ACTH in turn stimulates the synthesis and secretion of glucocorticoids from the adrenal gland (Hall, 2001). Increases in glucocorticoids following stress are critical for supporting metabolic, cardiovascular, immunologic and neural responses induced by threats to tissue viability and survival (Tsigos and Chrousos, 2002).…”

Section: Introductionmentioning

confidence: 99%

Differential regulation of parvocellular neuronal activity in the paraventricular nucleus of the hypothalamus following single vs. repeated episodes of water restriction-induced drinking

Arnhold

Wotus

Engeland

2007

Experimental Neurology

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Acute activation of the hypothalamic-pituitary-adrenal (HPA) axis releases glucocorticoids to maintain homeostasis, whereas prolonged exposure to elevated glucocorticoids has deleterious effects. Due to the potential benefits of limiting stress-induced glucocorticoid secretion, the present study uses drinking in dehydrated rats as a model to delineate mechanisms mobilized to rapidly inhibit HPA activity during stress. Using Fos expression as an indicator of neuronal activation, the effect of a single or repeated episode of dehydration-induced drinking on the activity of magnocellular and parvocellular neurons in the paraventricular nucleus (PVN) of the hypothalamus was examined. Adult male rats underwent a single episode or repeated (six) episodes of water restriction and were sacrificed before or after drinking water in the AM. Plasma osmolality, vasopressin (AVP), adrenocorticotropic hormone (ACTH) and corticosterone were elevated by water restriction and reduced after drinking in both models. Fos expression was elevated in AVP-positive magnocellular PVN neurons and AVP- and corticotropin releasing hormone (CRH)-positive parvocellular PVN neurons after water restriction. Fos expression was reduced in magnocellular AVP neurons after both models of restriction-induced drinking. In contrast, Fos expression did not change in AVP and CRH parvocellular neurons after a single episode of restriction-induced drinking, but was reduced after repeated episodes of restriction-induced drinking. These data indicate that drinking-induced decreases in glucocorticoids in dehydrated rats involve multiple factors including reduction in magnocellular release of vasopressin and reduction in parvocellular neuronal activity. The differential inhibition of PVN parvocellular neurons after repeated rehydration may reflect a conditioned response to repeated stress reduction.

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Actions of Corticotropin on the Adrenal Cortex: Biochemistry and Cell Biology

Cited by 5 publications

References 95 publications

Sympathetic nervous system contributes to enhanced corticosterone levels following chronic stress

Sympathetic nervous system contributes to enhanced corticosterone levels following chronic stress

Adrenal splanchnic innervation contributes to the diurnal rhythm of plasma corticosterone in rats by modulating adrenal sensitivity to ACTH

Differential regulation of parvocellular neuronal activity in the paraventricular nucleus of the hypothalamus following single vs. repeated episodes of water restriction-induced drinking

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