Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of interleukin-1 (IL-1) induces increases in plasma ACTH and glucocorticoids. Numerous experiments have implicated the hypothalamic CRH neurosecretory system in these responses, but have failed to provide evidence for involvement of the ACTH secretagogue vasopressin (VP). The rat CRH neurosecretory system contains two types of cells: VP expressing and VP deficient. Hence, the above findings suggested that IL-1 may selectively activate the VP-deficient subtype of CRH neurosecretory cells. In this study we employed postembedding electron microscopic immunocytochemistry to directly assay IL-1-induced depletion of secretory vesicles from identified VP-expressing and VP-deficient CRH neurosecretory axons. IL-1-induced depletion of secretory vesicles from these axons was correlated with increases in plasma ACTH and decreases in plasma PRL. No dose of IL-1 was found that could selectively activate one subtype of CRH neurosecretory axons; at doses of 0.67 microgram/100 g and above for both IL-1 alpha and IL-1 beta, equal depletion of vesicles from the two subtypes was observed. Similar results were previously found after the injection of bacterial lipopolysaccharide, which induces the release of IL-1 from macrophages. The findings unequivocally establish for the first time that IL-1 activates hypothalamic CRH neurosecretory cells in the absence of surgical stress, anesthesia, disruption of the infundibular area, or administration of toxic drugs. In addition, these data clearly demonstrate that IL-1 induces the release of VP from neurosecretory axons in the portal capillary zone of the external zone of the median eminence. Previous studies have shown that the VP-deficient subtype of CRH neurosecretory axons is not strongly activated by several types of stress; therefore, activation of the system by inflammatory mediators involves mechanisms different from those mediating the stress response.
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PMID:Effects of interleukin-1 on the stress-responsive and -nonresponsive subtypes of corticotropin-releasing hormone neurosecretory axons. 131 22

This in vitro study examined the effects of interleukin-1 (IL-1) and interferon-gamma (Ifn-gamma) on the release of cholecysto-kinin (CCK) from superfused hypothalamo-neurohypophyseal complexes (HNC) of rats. An increase of CCK from HNC was elicited in a dose-dependent manner by recombinant human IL-1 alpha and -1 beta in concentrations of 0.1-10 nM. In contrast, the release of CCK from HNC was not affected by recombinant human Ifn-gamma at any dose tested (0.1, 1 and 10 nM). The increased release of CCK elicited by IL-1 was calcium-dependent, as was that induced by potassium (60 mM), but it was biphasic and had a different time course and a lower magnitude than those induced by potassium and veratridine. These results suggest that IL-1 activates pituitary-adrenal axis by stimulating CCK neurons in the hypothalamus and/or neurohypophysis to release CCK, since CCK has been implicated in the regulation of adrenocorticotropin release.
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PMID:Stimulation of cholecystokinin (CCK) release from superfused rat hypothalamo-neurohypophyseal complexes by interleukin-1 (IL-1). 145 18

Arginine vasopressin (AVP) has previously been shown to participate in the neuroendocrine control of the adrenal axis. In this study we investigated the role of AVP in the mechanisms linking stress and decreased gonadotropin secretion and evaluated the action of an AVP antagonist on interleukin-1 alpha (IL-1 alpha)-induced changes in gonadotropin and cortisol release in the primate. Adult ovariectomized rhesus monkeys were given a 30-min intracerebroventricular infusion of IL-1 alpha (2.1 micrograms/30 min; n = 5) or IL-1 alpha plus an AVP antagonist (240 micrograms/120 min; [deamino-Pen1,O-Me-Tyr2,Arg8] vasopressin; n = 7); the AVP antagonist infusion was started 30 min before IL-1 alpha and continued for 2 h. Controls included intracerebroventricular infusions of physiological saline (n = 5) or AVP antagonist alone (n = 3). LH concentrations were measured at 15-min intervals during a 3-h preinfusion morning baseline control period and a 5-h postinfusion period. Cortisol concentrations were determined at 45-min intervals. Pulsatile LH release remained unchanged after a control saline or AVP antagonist infusion. Overall LH concentrations decreased significantly after IL-1 alpha infusion, from a morning control baseline of 109.9 +/- 8.8 to 53.7 +/- 3.2 ng/ml after the infusion (P less than 0.05). Concomitant infusion of the AVP antagonist prevented the IL-1 alpha-induced LH inhibition (morning control baseline, 144.5 +/- 6.8; postinfusion, 132.3 +/- 5.8; P = NS vs. saline; P less than 0.0001 vs. IL-1 alpha). While cortisol concentrations decreased throughout the experimental period in the animals receiving saline, they increased after IL-1 alpha infusion: mean +/- SE postinfusion cortisol concentrations were 29.6 +/- 1.9 micrograms/dl (saline) vs. 44.0 +/- 1.7 micrograms/dl (IL-1 alpha; P less than 0.0001). Coinfusion of AVP antagonist and IL-1 alpha did not block the IL-induced cortisol increase (46.8 +/- 1.5 micrograms/dl; P less than 0.0001 vs. morning). After the infusion of AVP antagonist alone, cortisol concentrations significantly decreased from a morning control value of 40.2 +/- 1.6 to 34.9 +/- 1.6 micrograms/dl (P less than 0.05). The results confirm our previous demonstration of an inhibitory effect of IL-1 alpha on gonadotropin secretion in the ovariectomized rhesus monkey and indicate for the first time an important inhibitory role for AVP in the control of gonadotropin secretion during stress. The data also suggest that in this species, the adrenocortical response to IL-1 does not require AVP.
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PMID:Vasopressin mediates the interleukin-1 alpha-induced decrease in luteinizing hormone secretion in the ovariectomized rhesus monkey. 161 95

We studied whether interleukin-1 (IL-1) affects the release of arginine vasopressin (AVP) from the superfused hypothalamo-neurohypophyseal complex (HNC) of rats. Involvement of the cholinergic system in the mediation of IL-1 on AVP release from HNC was also examined. Both human recombinant IL-1 alpha and -1 beta elicited a rapid increase of AVP from HNC in a dose-dependent manner at concentrations ranging from 0.1 to 10 nM. However, neither IL-1 alpha nor -1 beta at concentrations of 100 nM increased AVP, and even suppressed the stimulatory effect of 10 nM IL-1 alpha and -1 beta added later. Acetylcholine at concentrations of 1 to 100 nM caused a dose-dependent, rapid increase in AVP, whereas AVP release induced by 10 nM acetylcholine was completely suppressed by the combined presence of 10 microM hexamethonium, a nicotinic receptor antagonist, and 50 microM atropine, a muscarinic receptor antagonist. On the other hand, AVP release induced by 10 nM IL-1 alpha and -1 beta was not affected by the combination of the two antagonists. These results suggest that both IL-1 alpha and -1 beta may stimulate AVP release by acting directly on the hypothalamo-neurohypophyseal system, and that the stimulatory effect of IL-1 on AVP release may be independent of the cholinergic system.
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PMID:Interleukin-1 (IL-1) stimulates arginine vasopressin (AVP) release from superfused rat hypothalamo-neurohypophyseal complexes independently of cholinergic mechanism. 168 90

1. This study demonstrates that human recombinant interleukin-1 (IL-1) stimulates beta-endorphin release and potentiates the secretion of beta-endorphin in both a mouse anterior pituitary cell line AtT-20 and rat pituitary cell cultures. 2. In pituitary cell cultures, prolonged treatment with phorbol ester had no effect on IL-1-induced beta-endorphin release, but abolished the potentiating effects of IL-1 on vasopressin-induced beta-endorphin secretion. 3. The enhancement of CRF-stimulated beta-endorphin release by IL-1 was also reduced in normal pituitary cell cultures following depletion of protein kinase C. 4. The late IL-1-induced secretion of beta-endorphin does not require the continuous presence of the cytokine. 5. Incubation of monolayers with 125I-IL-1 alpha (10(-9) M) at 8 degrees C and then at 37 degrees C for various times revealed that IL-1 alpha was internalized. There was a progressive increase in the ratio of cytoplasmic to cell-surface-associated 125I-IL-1 alpha. 6. These results indicate that the IL-1-induced beta-endorphin release and its potentiation of beta-endorphin secretion involves internalization of this cytokine, perhaps via cell surface IL-1 receptors.
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PMID:Interleukin-1 potentiation of beta-endorphin secretion and the dynamics of interleukin-1 internalization in pituitary cells. 174 31

We demonstrated previously that interleukin-1 (IL-1) (recombinant human IL-1 alpha and -1 beta) stimulated the release of corticotropin-releasing factor (CRF) from the superfused rat hypothalamo-neurohypophyseal complex (HNC), independently of the cholinergic system. In the present study we studied the effects of IL-1 on the release of CRF not only from the HNC but also from the isolated hypothalamus of rats in a superfusion system to define the origin of measured CRF and the site of IL-1 action. We also studied the possible involvement of the histaminergic system in the mediation of the stimulation by IL-1. An increase in CRF was elicited from the HNC and the isolated hypothalamus in a dose-dependent manner by human recombinant IL-1 beta in concentrations of 0.1-10 nM with similar time courses. Histamine in concentrations of 1-100 nM also elicited qualitatively similar increases of CRF from these two types of explants. The increases in CRF release from the HNC induced by 10 nM of histamine were completely suppressed in the combined presence of pyrilamine (10 microM) and cimetidine (10 microM), an H1 and an H2 receptor antagonist, respectively. On the other hand, the increase in CRF release induced by 10 nM IL-1 beta was not affected by the combination of these two antagonists. These results indicate that IL-1 stimulates CRF release from the median eminence through an action on the hypothalamus, and that the stimulatory effect of IL-1 is probably independent of the histaminergic system.
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PMID:Interleukin-1 (IL-1) stimulates the release of corticotropin-releasing factor (CRF) from superfused rat hypothalamo-neurohypophyseal complexes (HNC) independently of the histaminergic mechanism. 178 43

Enhanced prostaglandin (PG) biosynthesis is a hallmark of inflammation, and interleukin-1 (IL), a proinflammatory cytokine, is a potent stimulus of PG production. We investigated the mechanisms of IL-1 alpha-enhanced PG synthesis in serum-stimulated mesangial cells. The rIL-1-stimulated increase in PGE2 synthesis was dose- and time-dependent and inhibited by both cycloheximide and actinomycin D. Phospholipase (PL) activity was increased 5- to 10-fold in acid extracts of rIL-1-treated cells as measured by arachidonate release from exogenous [14C]arachidonyl-phosphatidyl-ethanolamine. This induced phospholipase activity was Ca(2+)-dependent and inhibited by the PLA2 inhibitors, aristocholic acid, 7,7-dimethyl-5,8-eicosadienoic acid, and p-bromophenacylbromide, but not by the 1,2-diacylglycerol lipase inhibitor RHC 80267. The rIL-1-stimulated PLA2 had an alkaline pH optimum, and phosphatidylethanolamine was preferred over phosphatidylcholine as substrate. The PLA2 activity increased by rIL-1 was inhibited in cells coincubated with cycloheximide and was measurable after 6 h. A sensitive and specific solution hybridization assay demonstrated a coordinate time-dependent induction of non-pancreatic PLA2 mRNA expression which was increased at least 6-fold by 24 h. In whole cells, IL-1 had no effect on basal [3H]arachidonic acid release but vasopressin (1 microM)-stimulated release was potentiated 2- to 3-fold, suggesting that IL-1 may prime cells for increased PG synthesis via increased PLA2 activity. Thus IL-1 directly stimulates, as well as primes cells for, enhanced PG synthesis, in part, by increasing PLA2 activity through new synthesis of a non-pancreatic (Type II) PLA2.
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PMID:Interleukin-1 alpha stimulates prostaglandin biosynthesis in serum-activated mesangial cells by induction of a non-pancreatic (type II) phospholipase A2. 190 91

Interleukin-1 alpha (IL-1 alpha) exerts numerous neuroendocrinological and immunological actions. In the ovariectomized (OVX) monkey, intracerebroventricular (icv) infusion of IL-1 alpha stimulates the hypothalamo-pituitary-adrenal (HPA) axis and inhibits pulsatile LH and FSH secretion. This inhibitory effect of IL-1 alpha on the gonadotropins is prevented by coadministration of corticotropin releasing hormone (CRH) and vasopressin (AVP) antagonists, suggesting a role of these two HPA neuropeptides. In order to understand the central mechanisms by which "stress" interrupts the menstrual cycle, we have also investigated the modulatory role of estradiol. When early follicular phase estradiol concentrations are reproduced, there was a complete prevention of HPA activation and of the consequent inhibition of gonadotropin by IL-1 alpha. The mechanisms regulating this unexpected action remain to be elucidated. In contrast, in the presence of late follicular phase estradiol concentrations, the HPA response to IL-1 alpha is restored, but there is a stimulation of LH release. These data demonstrate interactions between the adrenal and gonadal endocrine axes, and highlight the role of estradiol in modulating these effects.
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PMID:The antireproductive role of corticotropin releasing hormone and interleukin-1 in the female rhesus monkey. 767 2

Arginine-vasopressin (AVP) has been previously shown to act in synergism with corticotropin-releasing hormone (CRH) in mediating stress-induced changes in the hypothalamo-pituitary-adrenal (HPA) axis. We have previously shown that both AVP and CRH play a role in mediating IL-1 alpha-induced changes in gonadotropin secretion. In this study, we investigate the effects of exogenously administered AVP on luteinizing hormone (LH) secretion in the ovariectomized (OVX) rhesus monkey. Adult OVX rhesus monkeys were given an intracerebroventricular (ICV) infusion of AVP (15 micrograms/h, n = 8; 50 micrograms/h, n = 5). Control animals received an ICV infusion of physiological saline at a rate 30 microliters/h (n = 12). LH concentrations were measured at 15-min intervals during a 3-hour preinfusion morning baseline and 5-hour postinfusion period. Cortisol concentrations were determined at 45-min intervals. Pulsatile LH release remained unchanged after a control saline infusion. After an AVP infusion, however, LH concentrations (ng/ml) significantly decreased (15 micrograms: from 172.9 +/- 6.4 baseline to 129.4 +/- 5.3; 50 micrograms: from 142.8 +/- 8.3 to 106.7 +/- 6.0, mean +/- SE; p < 0.05). By the fifth hour of the AVP infusion, areas under the LH curve were 64.3 +/- 10.5 and 62.9 +/- 11.0% of morning baseline for 15 and 50 micrograms hourly infusion rate, respectively. While cortisol concentrations decreased throughout the experimental period in the animals receiving saline (a.m.: 35.4 +/- 2.4 micrograms/dl vs. p.m.: 27.7 +/- 1.9 micrograms/dl), they increased after AVP infusion (15 micrograms/h: 42.3 +/- 2.4 vs. 54.6 +/- 2.0 micrograms/dl; 50 micrograms/h: 41.9 +/- 6.6 vs. 50.8 +/- 8.5 micrograms/dl).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibitory effect of arginine-vasopressin on LH secretion in the ovariectomized rhesus monkey. 820 13