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)

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

Numerous cells containing P-450(F-1) were detected in the magnocellular and parvocellular neurons of the paraventricular nucleus of the hypothalamus. Electron microscopic analysis of immunoreactive neurons has shown that P-450(F-1) immunoreactivity is present on the Golgi apparatus and rough endoplasmic reticulum. In the paraventricular nucleus, the P-450(F-1)-positive magnocellular neurons frequently contained oxytocin and some of them also contained CRF. Vasopressin was colocalized with P-450(F-1), but these neurons did not express CRF. In the supraoptic nucleus, P-450(F-1) was colocalized with oxytocin or CRF in single neurons, but not with vasopressin. No cells exhibiting the colocalization of both P-450(F-1) and somatostatin were observed in these nuclei. The results of the present study concerning colocalization of P-450 and peptides suggest that P-450(F-1) is involved in the hypothalamo-hypophyseal neuroendocrine function in the female rat.
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PMID:A sex-specific cytochrome P-450(F-1) colocalized with various neuropeptides in the paraventricular and supraoptic nuclei of female rats. 176 49

The present study has aimed to answer the following questions: 1) to what extent does the profile of volume related hormones in patients with chronic renal failure (CRF) differ from that of healthy subjects, and 2) do volume related hormones influence the electrolyte composition of thermal sweat? Twelve hemodialyzed patients with CRF and 20 healthy subjects were examined before and after one hour exposition to humid heat. In all examined subjects the following parameters were assessed before and after thermal dehydration: plasma renin activity (PRA) and plasma aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) concentrations. In addition sodium, potassium, and chloride were estimated in thermal sweat collected after 15 and 45 minutes respectively of thermal exposition. Patients with CRF showed significantly higher values of PRA, Ald, AVP and ANP before thermal dehydration. After one hour of heat exposition a significant increase in PRA, Ald and AVP but a significant decrease of plasma ANP level were noticed in both healthy subjects and patients with CRF. The magnitude of plasma Ald and ANP alterations induced by thermal dehydration was significantly more marked in patients than in healthy subjects. A similar electrolyte composition of thermal sweat was found in both examined groups. No significant correlation was found between the plasma profile of volume related hormones and electrolyte composition of sweat both in patients and normals. Results presented in this paper suggest, that volume related hormones do not influence the electrolyte composition of thermal sweat both in healthy subjects and patients with CRF.
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PMID:[Influence of thermal dehydration on blood values of hormones which regulate volume and composition of electrolytes in sweat of patients with ic renal failure treated with hemodialysis]. 181 85

Neuroendocrine activity in normal subjects was compared to patients with chronic renal failure on maintenance hemodialysis (CRF-HD) and to cyclosporine-treated renal transplantation (RT) recipients in an effort to further define the mechanisms underlying their associated fluid, electrolyte, and hemodynamic abnormalities. To evaluate neuroendocrine function in CRF and RT patients, plasma levels of angiotensin II (A-II), vasopressin (AVP), atrial natriuretic peptide (ANP), neuropeptide Y, neuropeptide Y (NPY), epinephrine (E), and norepinephrine (NE) were measured before and after HD and RT. Plasma concentrations of A-II, AVP, ANP, and NPY were significantly elevated in patients with CRF. HD did not produce a significant change in plasma concentrations of AVP, ANP, NPY, E, or NE. NE plasma levels, but not E levels, increased pre- and post-HD. A-II plasma levels were elevated basally in CRF patients and significantly increased following HD. Following RT, plasma levels of A-II, AVP, NPY, and creatinine decreased significantly over the first week, but AVP and NPY did not normalize. Plasma levels of ANP were elevated during the first month, then decreased to normal levels in RT patients. NE levels, but not E levels, were elevated both pre- and post-RT. Despite antihypertensive treatment, the group mean arterial pressure increased post-RT from 100 +/- 4.4 to 116 +/- 3.7 mmHg by POD 6.
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PMID:Neuroendocrinology of chronic renal failure and renal transplantation. 183 95

Bilateral adrenalectomy (ADX) leads to increased ACTH synthesis and secretion. It is thought that endogenous glucocorticoids exert a feedback mechanism at both pituitary and brain levels. The present study has been performed in order to determine the effect of ADX on the release of hypothalamic neuropeptides with corticotropin-releasing activity (CRA) and if there exists a median eminence site of glucocorticoid action to regulate hypothalamic-pituitary-adrenal (HPA) function. Adrenalectomized and sham-operated male rats were killed at different periods after surgery (2, 5, 7 and 14 days) and trunk blood was collected for ACTH and corticosterone (B) concentrations measurement. Brain (median eminence, ME; and medial basal hypothalamus, MBH) and pituitary (anterior lobe, AP; and neurointermediate lobe, NIL) tissues were dissected in order to evaluate either peptide content or in vitro hormone release. The results indicate that ADX blunted plasma B levels and increased AP ACTH content and secretion in a time-related fashion up to the 14th day. ADX significantly decreased both CRF and CRA contents in the ME at all periods studied; ME arginine-vasopressin (AVP) increased 7 and 14 days after ADX. MBH CRF decreased after ADX, but returned to sham value 2 weeks later; similarly, MBH AVP decreased at all periods after ADX. Removal of endogenous glucocorticoids did not vary neither oxytocin (OXY) content in the ME and MBH nor AVP and OXY contents in the NIL. In our superfusion experiments, we found that ADX increased basal AVP release and did not change spontaneous CRF secretion from ME terminals. Dexamethasone (Dxm, 10 nM) diminished AVP but not CRF output by ME tissues from adrenalectomized rats. A direct relationship was found between ME CRF and 28 mM KCl (hK+)-induced CRF release by MEs from adrenalectomized rats. ME fragments from adrenalectomized rats were hyperresponsive to kH+ stimulation of AVP release. Dxm (10 nM) decreased the hK(+)-evoked CRF and AVP release by MEs from adrenalectomized rats. ADX and dexamethasone treatment did not influence basal and hK(+)-elicited ME OXY release. Additionally, a rapid glucocorticoid inhibitory effect on ACTH secretion by isolated AP cells from both sham and adrenalectomized rats was found, and an in vitro corticotrope hyporesponse to 0.63 nM CRF and 9.25 nM AVP stimulation during several days after ADX.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Changes in the hypothalamo-corticotrope axis after bilateral adrenalectomy: evidence for a median eminence site of glucocorticoid action. 184 20

Influence of blockade converting enzyme on plasma renin activity (PRA), aldosterone and vasopressin secretion in 12 hemodialyzed patients with chronic renal failure and in 21 healthy subjects was observed. Our observation were provided during bed rest and water immersion tests. We didn't observe statistically significant influence PRA (increase after converting enzyme blockade) on vasopressin secretion in patients with chronic renal failure and in healthy subjects. Correlation between PRA and vasopressin secretion was absent.
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PMID:[Renin-angiotensin-aldosterone system (RAA) and vasopressin secretion in patients with chronic renal failure]. 189 92

There is considerable, although not entirely consistent, evidence that the hippocampus inhibits most aspects of HPA activity, including basal (circadian nadir) and circadian peak secretion as well as the onset and termination of responses to stress. Although much of the evidence for these effects rests only on the measurement of corticosteroids, recent lesion and implant studies indicate that the hippocampus regulates adrenocortical activity at the hypothalamic level, via the expression and secretion of ACTH secretagogues. Such inhibition results largely from the mediation of corticosteroid feedback, although more work is required to determine whether the hippocampus supplies a tonic inhibitory input in the absence of corticosteroids. It must be noted that the hippocampus is not the only feedback site in the adrenocortical system, since removal of its input only reduces, but does not abolish, the efficacy of corticosteroid inhibition, and since other elements of the axis appear eventually to compensate for deficits in feedback regulation. The importance of other feedback sites is further suggested not only by the presence of corticosteroid receptors in other parts of the brain and pituitary, but also by the improved prediction of CRF levels by combined hypothalamic and hippocampal receptor occupancy. The likelihood of feedback mediated by nonhippocampal sites underscores the need for future work to characterize hippocampal influence on HPA activity in the absence of changes in corticosteroid secretion. However, despite the fact that the hippocampus is not the only feedback site, it is distinguished from most potential feedback sites, including the hypothalamus and pituitary, by its high content of both type I and II corticosteroid receptors. The hippocampus is therefore capable of mediating inhibition over a wide range of steroid levels. The low end of this range is represented by corticosteroid inhibition of basal (circadian nadir) HPA activity. The apparent type I receptor specificity of this inhibition and the elevation of trough corticosteroid levels after hippocampal damage support a role for hippocampal type I receptors in regulating basal HPA activity. It is possible that basal activity is controlled in part through hippocampal inhibition of vasopressin, since the inhibition of portal blood vasopressin correlates with lower levels of hippocampal receptor occupancy, and the expression of vasopressin by some CRF neurons is sensitive to very low corticosteroid levels. At the high end of the physiological range, stress-induced or circadian peak corticosteroid secretion correlates strongly with occupancy of the lower affinity hippocampal type II receptors.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The role of the hippocampus in feedback regulation of the hypothalamic-pituitary-adrenocortical axis. 207 Jul 76

Water immersion (WI) induced alterations of plasma vasopressin (AVP), plasma osmolality, plasma volume (PV) and plasma sodium and potassium concentration were examined in 12 patients with noninflammatory acute renal failure (NARF) at the anuric/oliguric phase, 20 patients with chronic renal failure (CRF) and 15 healthy persons. In all examined groups a significant increase of PV and decrease of plasma osmolality and AVP after WI was observed. In patients with NARF the increase of PV was significantly greater than in CRF and in healthy persons. In patients with NARF a significantly greater decrease of plasma sodium concentration after WI was also noted than in patients with CRF and in healthy persons. Only in healthy persons, but not in patients with acute or chronic renal failure a significant correlation between PV or decrease of plasma osmolality and WI induced decrease of plasma AVP level was stated. We conclude that patients with NARF and CRF are characterized by an inappropriate volumetric and osmotic regulation of AVP secretion.
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PMID:Water immersion (WI) induced alterations of plasma vasopressin (AVP) levels in patients with noninflammatory acute renal failure (NARF) and in patients with chronic renal failure (CRF). 213 33

The concentration of beta-endorphin-immunoreactivity (beta E-IR) in cerebrospinal fluid (CSF) and plasma of rats was determined following intracerebroventricular (ICV) treatment of conscious animals with substances known to stimulate the release of beta E and other pro-opiomelanocortin (POMC)-derived peptides at the level of the anterior and intermediate lobes of the pituitary. The beta-adrenoceptor agoinst isoproterenol (ISO) did not influence the concentration of beta E-IR in CSF collected 5-60 min after ICV administration of doses ranging from 3 to 30,000 pg/rat. Plasma beta E-IR levels, however, were significantly increased 20 min following ICV injection of 30,000 pg ISO. ICV treatment of animals with ovine corticotropin-releasing factor (CRF; 30-30,000 pg/rat) also did not affect CSF levels of beta E-IR, whereas CRF in a dose of 30 pg significantly decreased, and in doses of 300-30,000 pg enhanced plasma beta E-IR concentrations as determined by 20 min following treatments. ICV injection of arginine8-vasopressin (AVP) in doses of 10-1,000 pg/rat dose-dependently elevated the beta E-IR concentration in CSF without affecting plasma beta E-IR levels. This AVP-induced increase in CSF beta E-IR was maximal 20-35 min and beta E-IR levels had returned to basal 60 min following treatment. The data indicate that AVP and not ISO and CRF is a stimulator of CSF levels of beta E-IR. As beta E-IR in CSF likely originates from brain POMC neurons, these results suggest the hot vasopressin may be a physiological regulator of brain POMC activity, and may act as a releasing factor for POMC-derived peptides in the brain.
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PMID:Effects of pituitary beta-endorphin secretagogues on the concentration of beta-endorphin in rat cerebrospinal fluid: evidence for a role of vasopressin in the regulation of brain beta-endorphin release. 213 62

Atrial natriuretic peptide, ANP(99-126), is derived from cardiac atrial tissue and has potent effects on salt and water homeostasis, including the inhibition of aldosterone and vasopressin release. Recent studies have also suggested that it may suppress the pituitary-adrenal axis. In addition, N-truncated forms of ANP, such as ANP(103-126), have been identified within the central nervous system, with a prominent hypothalamic localization in the paraventricular nucleus. We have therefore investigated whether ANP(99-126) and ANP(103-126) are able to modulate the release of the principal ACTH-releasing factor, corticotrophin-releasing factor-41 (CRF-41), from the rat hypothalamus in vitro. The static incubation system has been previously described in detail. Male Wistar rats were decapitated between 09.00 and 09.30 h, their hypothalami rapidly removed, and four half-hypothalami incubated for 20-min intervals following a period of stabilization. The effect of the ANP peptides on the basal (B) and KCl (28 mmol/l)-stimulated (S) release of immunoreactive CRF-41 was studied by means of successive incubations in the absence (B1, S1) and presence (B2, S2) of the peptides. The ratios B2:B1 and S2:S1 were compared with parallel control incubations by ANOVA. Neither form of ANP had any effect on the basal release of CRF-41. ANP(99-126) caused a dose-dependent inhibition of CRF-41 release in the concentration range 1-100 nmol (P less than 0.01). ANP(103-126) also suppressed the release of CRF-41 in the concentration range 100 pmol/l-100 nmol/l (P less than 0.01), with a minimum S2:S1 ratio at 10 nmol/l, and a decrease in effect at 100 nmol/l. Finally, the stimulation of CRF-41 release induced by noradrenaline (10 nmol/l and 1 mumol/l) was non-competitively antagonized by 100 nmol ANP(99-126)/l and 10 nmol ANP(103-126)/l.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptides inhibit the release of corticotrophin-releasing factor-41 from the rat hypothalamus in vitro. 214 72

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