UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The rapid secretion of ACTH in response to nicotine is mediated by a central mechanism involving brainstem catecholaminergic regions. To identify specific brainstem regions involved in activating the hypothalamo-pituitary-adrenal axis and other areas of the brain by iv nicotine, immunocytochemical detection of cFos protein was used as a marker for neuronal activation. Nicotine (0.05 mg/kg) stimulated cFos expression in the parvocellular paraventricular nucleus (pcPVN; containing CRH-positive neurons mediating ACTH secretion); this correlated with the expression of cFos in the A2 (norepinephrinergic) and C2 (epinephrinergic) regions of the brainstem nucleus tractus solitarius, which project directly to the pcPVN. The selectivity of this brainstem activation was shown by the absence of responses in the locus coeruleus (LC), A1, and C1 catecholaminergic regions to this low dose of nicotine. In contrast, a high dose of nicotine (0.1 mg/kg), which produced a brief episode of tremor, was required for expression of cFos in the LC. This was associated with a further increase in the number of cFos-positive cells in the PVN, primarily through recruitment in the magnocellular region, a known projection field of LC. The higher dose of nicotine also induced cFos in the vasopressinergic region of the supraoptic nucleus (SON), whereas the lower dose of nicotine exclusively induced cFos in the oxytocinergic region of the SON. Limbic regions that receive catecholaminergic inputs, such as the the central nucleus of the amygdala (involved in PVN regulation) and the cingulate gyrus of the cortex, showed a dose-dependent increase in the number of cFos-positive cells after nicotine, whereas the dentate gyrus of the hippocampus only responded to the high dose. Thus, nicotine is a potent and selective stimulus for neuronal activation in brainstem catecholaminergic regions and their projection fields in the pcPVN and SON, which regulate the hypothalamo-pituitary-adrenal axis and vasopressin/oxytocin secretion, respectively.
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PMID:Nicotine stimulates the expression of cFos protein in the parvocellular paraventricular nucleus and brainstem catecholaminergic regions. 838 11

The hypothalamic hypophysiotrophic neurones are densely innervated by adrenergic and noradrenergic nerve terminals. Activation of alpha 1-adrenoceptors located in the brain stimulates the secretion of ACTH, prolactin and TSH. The effects of the alpha 1-adrenoceptors seem to be exerted on hypothalamic neurones that secrete vasopressin, CRH-41 and TRH. These mechanisms are important in the physiological control of the secretion of ACTH and TSH in humans. alpha 2-Adrenoceptors are not involved in the control of secretion of these hormones under basal conditions in humans. However, alpha 2-adrenoceptors exert an inhibitory effect that acts as a negative feedback mechanism, limiting excessive secretion of these hormones. There is no convincing evidence for the involvement of beta-adrenoceptors in the control of the secretion of these three hormones in humans. Studies on cultured anterior pituitary cells suggested that adrenaline and noradrenaline may influence the secretion of ACTH, prolactin and TSH directly at the level of the pituitary. However, these effects are not demonstrable in humans, and are likely to be due to alterations in the pituitary adrenoceptors during culture. In the case of growth hormone, activation of alpha 2-adrenoceptors located in the brain stimulates secretion of this hormone both by increasing the secretion of GHRH and by inhibiting the secretion of somatostatin. Activation of beta-adrenoceptors inhibits the secretion of growth hormone via an increase in the secretion of somatostatin. The effects of the central alpha 2- and beta-adrenoceptors are important in the physiological control of growth hormone secretion in humans. A considerable amount of evidence implicates brain alpha 1-adrenoceptors in the control of secretion of the gonadotrophins in experimental animals, but, despite intensive study, no convincing evidence has been found in humans of reproductive age.
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PMID:Adrenergic control of the secretion of anterior pituitary hormones. 838 73

Plasma ACTH and cortisol concentrations are frequently elevated in patients in intensive care units (ICU). To examine the functional integrity of the hypothalamic-pituitary-adrenal axis during critical illness, we evaluated prospectively 53 ICU patients in a general medical ICU. Thirty-one patients and 7 normal controls underwent an overnight dexamethasone suppression test (3 mg dexamethasone, orally, at 2300 h). Plasma ACTH and serum cortisol were measured at 0900 h. In a separate experiment, 22 patients and 7 control subjects underwent a CRH stimulation test [100 micrograms human (h) CRH, iv]. ACTH and cortisol concentrations were determined from -15 to 120 min. Compared to normal controls, plasma ACTH and serum cortisol concentrations were not fully suppressible by dexamethasone [mean +/- SEM: plasma ACTH, 21 +/- 4 vs. 3 +/- 0.5 pg/mL (4.7 +/- 0.9 vs. 0.7 +/- 0.1 pmol/L); serum cortisol, 13.9 +/- 1.9 vs. 1.5 +/- 0.3 micrograms/dL (390 +/- 50 vs. 40 +/- 10 nmol/L); P = 0.0001], demonstrating an altered glucocorticoid feedback in the ICU patients. Patients undergoing hCRH stimulation had clearly elevated mean baseline plasma ACTH and serum cortisol concentrations [ACTH, 78 +/- 20 pg/mL vs. 15 +/- 3 in controls (17.2 +/- 4.4 vs. 3.4 +/- 0.7 pmol/L; P = 0.007); cortisol, 36.8 +/- 3.4 micrograms/dL vs. 9.6 +/- 1.2 (1020 +/- 80 vs. 260 +/- 30 nmol/L; P = 0.0001)]. Despite elevated baseline glucocorticoid concentrations, stimulation with hCRH resulted in significantly higher peak plasma ACTH concentrations 15 min after hCRH than in controls [134 +/- 31 vs. 48 +/- 9 pg/mL (29.5 +/- 6.8 vs. 10.6 +/- 2.0 pmol/L); P < 0.05]. Serum cortisol concentrations in ICU patients were significantly elevated throughout the test period (P = 0.0001) and rose to a peak of 43.9 +/- 3.5 micrograms/dL compared to 18.2 +/- 2.0 micrograms/dL in controls (1210 +/- 70 vs. 500 +/- 60 nmol/L). We conclude that ICU patients have a markedly altered responsiveness of their pituitary corticotroph to suppression with dexamethasone and stimulation with hCRH. These findings may be explained by altered pituitary glucocorticoid feedback and/or hypersecretion of peptides with CRH-like activity (vasopressin and cytokines) during critical illness.
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PMID:The hypothalamic-pituitary-adrenal axis in critical illness: response to dexamethasone and corticotropin-releasing hormone. 839 81

The physiological regulation of ACTH secretion is largely dependent on the interactive effects of CRH and vasopressin (VP) in the pituitary corticotroph. The importance of the magnocellular and parvicellular hypothalamic systems as a source of VP for pituitary regulation was studied by analyzing the effects of endogenous activation of these systems or VP infusion on the ability of CRH to regulate its receptor sites in the anterior pituitary. CRH receptors were measured by binding of [125I]Tyr-ovine CRH to membrane-rich fractions of anterior and neurointermediate pituitary lobes. Minipump infusion of 100 ng/min CRH for 48 h caused a 40% decrease in the anterior pituitary CRH receptor concentration. Simultaneous infusion of VP markedly potentiated the effect of CRH, but only at doses that elevated plasma VP to levels in the range of those in the pituitary portal circulation. Activation of the magnocellular vasopressinergic system by 60 h of water deprivation increased plasma VP levels from 0.5 +/- 0.1 to 11.8 +/- 0.6 pg/ml, but had no effect on the anterior pituitary CRH receptor concentration in control rats or animals receiving CRH infusion (100 ng/min for 48 h). The CRH receptor concentration was significantly increased in neurointermediate pituitary membranes from water-deprived rats. When the parvicellular vasopressinergic system was activated by 14 days of repeated restraint stress, there was a significant enhancement in the ability of CRH to decrease anterior pituitary CRH receptors (33% and 62% in control and stressed rats, respectively). The concomitant infusion of 200 ng/min of the VP antagonist [(mercapto cyclopentamethylene propionic acid)-[methyl-tyrosine]arginine VP] during the CRH infusion in chronically stressed rats significantly reduced the magnitude of the pituitary CRH receptor loss from a 62% to a 43% decrease (P < 0.01). In conclusion, exogenous VP modulates pituitary CRH receptor regulation by CRH only at doses sufficiently high to provide peripheral VP concentrations in the range of the circulating levels in hypophysial-portal blood. Furthermore, the demonstration that chronic endogenous activation of the parvicellular, but not the magnocellular, vasopressinergic system enhances the down-regulatory effect of CRH on anterior pituitary CRH receptors is in support of a critical role of parvicellular VP in the control of the corticotroph function.
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PMID:Regulation of pituitary corticotropin releasing hormone (CRH) receptors by CRH: interaction with vasopressin. 840 13

A number of recent studies suggest that cells of the immune system, e.g. peripheral blood mononuclear cells (PBMC), can synthesize and process POMC and secrete POMC-derived peptides, such as ACTH and endorphins, upon immune and hormonal challenges. From this, it has been proposed that POMC-derived peptides originating from lymphoid cells can function as hormones, for instance in a lymphoid-adrenal axis. In view of the important physiological implications of this proposal, the present study was designed to investigate the expression of the POMC gene in human PBMC and the production by these cells of alpha-, beta-, and gamma-endorphins (alpha E, beta E, and gamma E) peptides that are established end products of the posttranslational processing of POMC. PBMC of individual donors were used uncultured (fresh cells) or cultured for 24 and 48 h in the presence and absence of Concanavalin-A (Con-A), bacterial lipopolysaccharide, phytohemagglutinin, or CRH, and vasopressin, conditions that reportedly stimulate POMC activity in those cells, to investigate the presence of POMC transcripts by analysis of total RNA with Northern blotting and the reverse transcriptase polymerase chain reaction (RT-PCR). Large scale preparations containing over 10(9) cells (fresh, cultured with and without Con-A) originating from several donors were examined for the presence of POMC transcripts by analysis of poly(A)+ RNA on Northern blots and for the presence of alpha E, beta E, and gamma E by gel filtration over Sephadex G-75 and reverse phase HPLC, followed by assay of the fractions in four endorphin RIA systems with different specificities. On the Northern blots of total RNA, no POMC transcripts were detectable. In poly(A)+ RNA preparations, no full-length POMC mRNA was found, and it was estimated that the concentration of POMC mRNA, if present, was below approximately 0.005 transcript/cell in Con-A-stimulated cells and still lower in unstimulated cells. In accord with literature data, an 800- to 900-nucleotide POMC transcript was detected in cultured PBMC, and the levels of this transcript were stimulated by Con-A. In all samples analyzed with RT-PCR, a transcript spanning most of exons 2 and 3 was detectable only on Southern blots of the RT-PCR product, but not on agarose gels stained with ethidium bromide. Chromatographic analysis of endorphin immunoreactivities in cell extracts revealed no qualitative differences between the immunoreactive profiles of fresh PBMC or PBMC cultured with or without Con-A.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Analysis of proopiomelanocortin (POMC) messenger ribonucleic acid and POMC-derived peptides in human peripheral blood mononuclear cells: no evidence for a lymphocyte-derived POMC system. 840 37

The secretion of neurohypophyseal hormone and ACTH in the rat has been shown to exhibit circadian rhythms, with high values during the day and low values throughout the night. The neurohypophyseal hormone daily rhythm is altered by exposure to constant light and by pinealectomy. It was, thus, proposed that the observed fall in vasopressin (AVP), oxytocin, and ACTH over the hours of darkness could be related to the release of melatonin seen at this time. Therefore, a study was performed to determine the effect of melatonin on AVP, oxytocin, and CRH-41 release from the isolated rat hypothalamus in vitro. Employing a previously validated technique, rat hypothalami were incubated in either medium alone or medium containing melatonin or one of two melatonin analogs. Hormone release was measured by RIA, and the ratios were calculated and compared by Student's t test, with Dunnett's correction for multiple comparisons. Melatonin showed a dose-dependent inhibition of both basal and stimulated AVP and oxytocin release in the concentration range 4.3 x 10(-10) to 2.5 x 10(-3) M, while having no significant effect on the release of CRH-41. The two melatonin analogs, 2-iodomelatonin and 5-methoxy-N-isobutanoyltryptamine, were also found to inhibit both basal AVP and oxytocin release, indicating that this effect probably depends upon the presence of melatonin receptors in the hypothalamus. This inhibitory modulation of AVP, in the absence of any effect on CRH-41, suggests that melatonin may affect water balance by means of directly inhibiting hypothalamic AVP release. Furthermore, circadian rhythmicity in pituitary-adrenal activity may depend on melatonin modulation of AVP, rather than changes in CRH-41.
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PMID:Melatonin and its analogs inhibit the basal and stimulated release of hypothalamic vasopressin and oxytocin in vitro. 844 Jan 90

Previous studies have demonstrated that acute stress or ovine corticotropin-releasing hormone (oCRH) in vivo, or oCRH in vitro, stimulates release of beta-endorphin over beta-lipotropin from anterior pituitary corticotropes. This occurs despite the predominance of beta-lipotropin in corticotrope peptide stores. In vitro studies with primary anterior pituitary cultures suggested that chronic exposure to oCRH results in a shift towards more beta-lipotropin secretion into the media than with short-term exposure. The current studies explored whether increased secretory drive in vivo results in a similar shift towards more beta-lipotropin. We used removal of glucocorticoids by adrenalectomy or metyrapone blockade of corticosterone synthesis, to stimulate endogenous secretion of CRH and vasopressin. Both treatments resulted in shifts of the ratio of beta-endorphin: beta-lipotropin in plasma of experimental animals in comparison to the sham-treated control rats. In vitro testing with oCRH of anterior lobe cultures from adrenalectomized or metyrapone-treated rats demonstrated similar effects of these treatments on the ratio of beta-endorphin:beta-lipotropin. These changes occurred despite similar ratios of beta-endorphin:beta-lipotropin in anterior pituitary peptide stores.
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PMID:Altered ratios of beta-endorphin: beta-lipotropin released from anterior lobe corticotropes with increased secretory drive. I. Effects of diminished glucocorticoid secretion. 848 40

Hypocortisolism derived from hypothalamic deficiency of corticotropin releasing hormone is a highly unusual cause of adrenal insufficiency, and its pathogenesis is still not fully understood. We report a mildly symptomatic patient having repeated low basal plasma cortisol levels with normal cortisol response to ACTH and Lysine-vasopressin; however, she showed a clearly limited response to deep hypoglycemia, while GH reached a normal concomitant response. After 7 years of cortisol replacement the endogenous cortisol returned spontaneously to normality. The rest of pituitary function has been always normal.
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PMID:[Hypocorticism due to selected deficiency of CRH with spontaneous resolution. A case report]. 852 75

The significance of adrenergic neurons and anterior pituitary and hypothalamic adrenergic receptors in stimulation of the hypothalamic-pituitary-adrenal (HPA) axis by corticotropin releasing hormone (CRH) and vasopressin (AVP) was investigated under basal conditions and after three-days crowding stress in conscious rats. In nonstressed rats the corticosterone response to phenylephrine, an alpha 1-adrenergic receptor agonist, was totally abolished or considerably reduced by prazosin, an alpha 1-receptor antagonist, when both those drugs were given ip or icv, respectively. The corticosterone response to ip isoproterenol, a beta-adrenergic agonist, was abolished by icv or ip pretreatment with propranolol, a beta-adrenergic receptor antagonist. These results indicate involvement of functional alpha 1-adrenoceptors in the hypothalamus and anterior pituitary corticotrops and pituitary beta-adrenoceptors in stimulation of the HPA axis. AVP given ip was almost as potent as CRH in stimulating corticosterone secretion. The stimulatory effect of AVP given ip or icv on corticosterone secretion was significantly diminished by propranolol, but not prazosin or yohimbine, indicating an involvement of beta-adrenergic receptors. The specific noradrenergic neurotoxin DSP-4, given ip 11 days before the experiment, considerably diminished the hypothalamic noradrenaline (NA) level but did not influence the resting and icv CRH- or AVP-stimulated corticosterone secretion. In nonstressed rats CRH further enhanced significantly the DSP-4-elicited fall in hypothalamic NA, whereas AVP almost totally prevented that decrease. In stressed rats CRH considerably antagonized the DSP-4-induced decrease in the hypothalamic NA level while AVP did not affect that decrease. The CRH- and AVP-elicited changes in hypothalamic NA were not correlated with changes in corticosterone secretion. Tree-day crowding stress did not affect the CRH-induced corticosterone secretion, whereas it considerably reduced the AVP-evoked corticosterone response. These results indicate that pituitary and hypothalamic adrenergic receptors are significantly involved in the AVP- and CRH-induced HPA axis stimulation, but the hypothalamic NA level, though modified by these peptides, does not significantly influence the HPA response.
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PMID:Adrenergic regulation of the hypothalamic-pituitary-adrenal axis under basal and social stress conditions. 852 11

1. Healthy male volunteers were exposed to either a heat condition (52 degrees C) or normal temperature (28 degrees C) receiving a single oral dose of 3 mg haloperidol or placebo in a double-blind design. 2. Ratings on aversiveness as well as on intensity of ambient temperature and saliva samples for determination of cortisol were sampled at defined intervals. Body core temperature and sweat loss were measured continuously throughout the three hour experiment. 3. Results indicate increased levels of cortisol after exposure to heat but not after a pretreatment with haloperidol. 4. The findings of this study suggest that D2-receptors of tuberoinfundibular neurons are blocked by haloperidol which suppresses the dopamine mediated release of vasopressin induced by dehydration and the subsequent stimulation of CRH.
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PMID:Suppression of HPA-axis activity by haloperidol after experimentally induced heat stress. 858 59

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