Effects of interleukins on plasma arginine vasopressin and oxytocin levels in conscious, freely moving rats

Naito, Yoshiyuki; Fukata, Junichi; Shindo, Kazuo; Ebisui, Osamu; Murakami, Norihiko; Tominaga, Tomoko; Nakai, Yoshikatsu; Mori, Kenjiro; Kasting, Norman W.; Imura, Hiroo

doi:10.1016/0006-291x(91)91547-p

Cited by 83 publications

(54 citation statements)

References 14 publications

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“…However, the influence of LPS and cytokines on AVP release remains controversial. 127,136,222,223 In another study in unrestrained conscious sheep, Dadoun et al demonstrated that the activation of the HPA axis after endotoxin administration is associated with an increased release of both CRH and AVP into hypophysial portal blood (HBP). 224 Magnocellular AVP neurons are only initially stimulated, while parvocellular CRH and AVP neurons are stimulated throughout these experiments, as reflected by different AVP levels in portal and jugular blood.…”

Section: Non-cytokine Pathways: Cyclo-oxygenase Avp Leptin Estrogementioning

confidence: 99%

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Beishuizen

Thijs

2003

Journal of Endotoxin Research

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Endotoxin is considered to be a systemic (immunological) stressor eliciting a prolonged activation of the hypothalamo-pituitary-adrenal (HPA) axis. The HPA-axis response after an endotoxin challenge is mainly due to released cytokines (IL-1, IL-6 and TNF-a) from stimulated peripheral immune cells, which in turn stimulate different levels of the HPA axis. Controversy exists regarding the main locus of action of endotoxin on glucocorticoid secretion, since the effect of endotoxin on this neuro-endocrine axis has been observed in intact animals and after ablation of the hypothalamus; however, a lack of LPS effect has been described at both pituitary and adrenocortical levels. The resulting increase in adrenal glucocorticoids has well-documented inhibitory effects on the inflammatory process and on inflammatory cytokine release. Therefore, immune activation of the adrenal gland by endotoxin is thought to occur by cytokine stimulation of corticosteroidreleasing hormone (CRH) production in the median eminence of the hypothalamus, which, in turn stimulates the secretion of ACTH from the pituitary. Acute administration of endotoxin stimulates ACTH and cortisol secretion and the release of CRH and vasopressin (AVP) in the hypophysial portal blood. During repeated endotoxemia, tolerance of both immune and HPA function develops, with a crucial role for glucocorticoids in the modulation of the HPA axis. A single exposure to a high dose of LPS can induce a long-lasting state of tolerance to a second exposure of LPS, affecting the response of plasma TNF-a and HPA hormones. Although there are gender differences in the HPA response to endotoxin and IL-1, these responses are enhanced by castration and attenuated by androgen and estrogen replacement. Estrogens attenuate the endotoxin-induced stimulation of IL-6, TNF-a and IL-1ra release and subsequent activation in postmenopausal women. There appears to be a temporal and functional relation between the HPA-axis response to endotoxin and nitric oxide formation in the neuro-endocrine hypothalamus, suggesting a stimulatory role for nitric oxide in modulating the HPA response to immune challenges. demonstrate higher plasma levels of IL-1 and TNF-a. Elevation of plasma glucocorticoids results in suppression of cytokines such as IL-1, IL-6, and TNF-a and in up-regulation of other cytokines, such as IL-4 and IL-10, and cytokine receptors. Thus, by regulation of cytokine production and action, the HPA axis contributes to modulation of the response to inflammation/infection. In addition, the role of HPA activation has been suggested to be a negative feedback system provided by the immunosuppressive activity of glucocorticoids, limiting inflammatory responses and preventing the immune system from over-reacting and causing tissue damage or autoimmunity.As early as 1957, Wexler et al. suggested that LPS could induce ACTH release since they found a depletion of ascorbic acid and cholesterol in the adrenal glands. 10 Moreover, LPS was not able to cause these changes in hypophysectomized rats. ...

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Section: Non-cytokine Pathways: Cyclo-oxygenase Avp Leptin Estrogementioning

confidence: 99%

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Beishuizen

Thijs

2003

Journal of Endotoxin Research

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“…Recently it was reported that interleukin (IL)-l p stimulates the secretion of corticotropin releasing hormone, ACTH and corticosteroid (17), and induces an increase in the level of ADHin rats (18). The present case experienced eczema on the trunk and extremities whenshe had eaten raw shiitake mushrooms as a private remedy.…”

Section: Discussionmentioning

confidence: 67%

Severe Hyponatremia Caused by Hypothalamic Adrenal Insufficiency.

1999

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A 60-year-old womanwas admitted with severe hyponatremia. Basal values of adrenocorticotropic hormone (ACTH), thyroid hormone and cortisol were normal on admission. Impairment of water diuresis was observed by water loading test. Initially, we diagnosed her condition as the syndrome of inappropriate secretion of antidiuretic hormone(SIADH). By provocation test, we finally confirmed that the hyponatremia was caused by hypothalamic adrenal insufficiency. The basal values ofACTHand cortisol might not be sufficient to exclude the possibility of adrenal insufficiency. Therefore, it is necessary to evaluate adrenal function by provocation test or to re-evaluate it after recovery from hyponatremia. (Internal Medicine 38: 426-432, 1999)

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“…Plasma AVPlevels were also elevated, suggesting that IL-6 activated the magnocellular AVPsecreting neurons, and it may be involved in SIADH. Cytokines are known to exhibit a hormone-like action, and they stimulate the secretion of corticotropin-releasing hormoneand anti-diuretic hormone (ADH) (5,6). Accordingly, the immune system is considered to participate in regulating the homeostasis of body fluids by affecting neuroendocrine mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…It is knownthat immuneresponses are associated with a variety ofendocrine activities (4). Interleukin (IL)-l , IL-6, and tumor necrosis factor (TNF)-acan stimulate the synthesis and secretion of corticotropin-releasing hormoneand vasopressin directly in rats (5,6). Furthermore, it has been confirmed that intravenous administration of recombinant IL-6 stimulates AVPsecretion through a nonosmotic mechanism in man (7).…”

Section: Introductionmentioning

confidence: 99%

Hyponatremia in a Patient with Chronic Inflammatory Disease.

et al. 1998

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A 66-year-old man was admitted with destructive arthropathy, and calcium pyrophosphate dihydrate was demonstrated in the synovial fluid specimen. He was found to have a hyponatremia. The serum sodium concentration was 121 mmol//, plasma arginine vasopressin (AVP) 6.6 pmol//, and serum interleukin (IL)-6 96 pg//. The clinical findings suggest the diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH). However, destructive arthropathy with increased values of C-reactive protein and IL-6 is the only background of SIADHin this patient. We suggest the possibility that IL-6 produced at inflammatory lesions may have stimulated an excessive release of AVPresulting in the hyponatremia and hypochloremia of SIADH. (Internal Medicine 37: 792-795, 1998)

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Effects of interleukins on plasma arginine vasopressin and oxytocin levels in conscious, freely moving rats

Cited by 83 publications

References 14 publications

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Review: Endotoxin and the hypothalamo-pituitary-adrenal (HPA) axis

Severe Hyponatremia Caused by Hypothalamic Adrenal Insufficiency.

Hyponatremia in a Patient with Chronic Inflammatory Disease.

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