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 effects of chronic immune challenge on cytokine expression and hypothalamic-pituitary-adrenal axis (HPA) axis responses to stress were studied in Wistar rats after administration of increasing doses of lipopolysaccharide (LPS). Repeated LPS (R-LPS) decreased body weight and increased adrenal weight and pituitary pro-opiomelanocortin mRNA levels. LPS injection increased plasma adrenocorticotropic hormone (ACTH) and corticosterone but the effect was attenuated in R-LPS. Plasma corticosterone but not ACTH responses to restraint were also reduced in R-LPS. Basal and restraint-stimulated corticotropin releasing hormone (CRH) mRNA levels were lower in R-LPS, but responses to a new LPS injection were similar to controls. In contrast, type 1 CRH receptor (CRH-R1) mRNA responses to both LPS and restraint were blunted in R-LPS. Vasopressin mRNA levels in parvocellular neurones were higher in R-LPS, and increased further after restraint but not after a new LPS injection. Glucocorticoid receptor (GR) levels in the paraventricular nucleus (PVN) increased after a single LPS or R-LPS (24 h after the last injection) but declined after a new injection in R-LPS. Interleukin (IL)-1beta and IL-6 mRNAs increased in the pituitary, spleen and circumventricular organs after single or R-LPS, suggesting that cytokines may contribute to the activation of the HPA axis though pathways from the circumventricular organs as well as paracrine effects in the pituitary. The data show that (i) adaptation of the HPA axis during repeated LPS injection involves increases in vasopressin : CRH expression ratios in parvocellular neurones; (ii) that hypothalamic CRH and vasopressin responses to acute stimulation are independent of CRH-R1 expression in the PVN; and (iii) there is a dissociation between pituitary and adrenal responses to acute stress suggesting a decrease of adrenal sensitivity to ACTH.
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PMID:Effect of repeated lipopolysaccharide administration on tissue cytokine expression and hypothalamic-pituitary-adrenal axis activity in rats. 1148 88

The differential effects of osmotic stimulation on magnocellular and parvocellular hypothalamic neurons were studied by analysis of corticotropin-releasing hormone (CRH) and vasopressin (VP) expression in controls and 48-h water-deprived rats subjected to either restraint for 1 h or a single lipopolysaccharide injection (250 microg/100 g). Water deprivation reduced basal CRH mRNA levels but the increments following 4 h of restraint or 6 h lipopolysaccharide (LPS) injection were similar to those in controls. In contrast, water deprivation had no effect on basal VP heteronuclear RNA (hnRNA) and mRNA levels in parvocellular neurons, but responses to restraint or LPS injection were reduced. VP expression in magnocellular paraventricular and supraoptic nuclei, and plasma sodium and vasopressin were higher in water-deprived rats, changes which were unaffected by restraint. LPS injection reduced VP mRNA but not hnRNA levels in magnocellular neurons and increased plasma vasopressin levels only in water-deprived rats independently of changes in plasma sodium. This was accompanied by an increase in vasopressin mRNA content in the posterior pituitary. The data show that the blunted ACTH responses to acute stress during chronic osmotic stimulation are correlated with the inability of parvocellular neurons to increase VP rather than CRH expression. In addition, LPS-induced endotoxemia causes disturbances of the magnocellular vasopressinergic system with an unexpected potentiation of osmotic simulated VP secretion. The lack of increase in VP transcription after LPS and changes in VP mRNA distribution suggest that endotoxemia affect the secretory process at the levels of the neurohypophyseal axon terminal.
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PMID:Hypothalamic pituitary adrenal axis and hypothalamic-neurohypophyseal responsiveness in water-deprived rats. 1157 86

Pathogenesis of febrile convulsions (FC) is still unknown, suggested causes include the role of antidiuretic hormone (ADH). ADH is an endogenous antypyretic and his excessive production of the consequent hyponatraemia may be the cause of FC in children with susceptibility to this type of seizure. Whereas, interleukin-1 (IL1) is a pyrogenic substances and is involved in the release of AVP. Helminen et al. have reported a significantly higher production of IL1 in culture of peripheral blood monocytes stimulated with lipopolysaccharide (LPS) of children with FC than in the others with fever but without convulsions. More recently Lahat et al. have compared plasma and cerebrospinal fluid ILI levels of children with FC with those of children with fever but without convulsions, but they did not find significant differences. The aims of this study were to determine the IL1 levels in vivo and in the supernatants of cultures of peripheral blood mononuclear cells (PBMC) stimulated or not with LPS in children with FC and in children with fever without FC and to evaluate the influence of ADH and diazepam (DZ) on IL1 production. Blood samples for PBMC cultures were obtained from 11 children with FC on the hospital admission, (group 1) and after 48 hours from treatment with DZ (group 2). The production of IL1 was measured by RIA in the supernatants of the PBMC stimulated with LPS, LPS + DDAVP (synthetic vasopressin), LPS + DZ and in vivo in plasma samples. The control groups were constituted by 9 children with fever and without convulsions (group 3), 4 of them were studied at the end of fever too (group 4), and finally by 9 children in good health (group 5). No significant differences were observed. These results do not support the hypothesis that increased production of IL1 is involved in the pathogenesis of FC in children.
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PMID:[In vivo and in vitro production of interleukin-1 after febrile convulsions]. 1159 68

The reduced pressure response to vasopressin during acute sepsis has directed our interest to the regulation of vasopressin V(1A) receptors. Rats were injected with lipopolysaccharide for induction of experimental gram-negative sepsis. V(1A) receptor gene expression was downregulated in the liver, lung, kidney, and heart during endotoxemia. Inasmuch as the concentrations of proinflammatory cytokines such as interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma were highly increased during sepsis, the influence of these cytokines on V(1A) receptor expression was investigated in primary cultures of hepatocytes and in the aortic vascular smooth muscle cell line A7r5. V(1A) receptor expression was downregulated by the cytokines in a nitric oxide-independent manner. Blood pressure dose-response studies after injection of endotoxin showed a diminished responsiveness to the selective V(1) receptor agonist Phe(2),Ile(3),Orn(8)-vasopressin. Our data show that sepsis causes a downregulation of V(1A) receptors and suggest that this effect is likely mediated by proinflammatory cytokines. We propose that this downregulation of V(1A) receptors contributes to the attenuated responsiveness of blood pressure in response to vasopressin and, therefore, contributes to the circulatory failure in septic shock.
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PMID:Cytokine-mediated downregulation of vasopressin V(1A) receptors during acute endotoxemia in rats. 1189

In conscious, chronically instrumented rats we examined 1) renal tubular functional changes involved in lipopolysaccharide (LPS)-induced acute renal failure; 2) the effects of LPS on the expression of selected renal tubular water and sodium transporters; and 3) effects of milrinone, a phosphodiesterase type 3 (PDE3) inhibitor, and Ro-20-1724, a PDE4 inhibitor, on LPS-induced changes in renal function. Intravenous infusion of LPS (4 mg/kg b.wt. over 1 h) caused an immediate decrease in glomerular filtration rate (GFR) and proximal tubular outflow without changes in mean arterial pressure (MAP). LPS-induced fall in GFR and proximal tubular outflow were sustained on day 2. Furthermore, LPS-treated rats showed a marked increase in fractional distal water excretion, despite significantly elevated levels of plasma vasopressin (AVP). Semiquantitative immunoblotting showed that LPS increased the expression of the Na(+),K(+),2Cl(-)-cotransporter (BSC1) in the thick ascending limb, whereas the expression of the AVP-regulated water channel aquaporin-2 in the collecting duct (CD) was unchanged. Pretreatment with milrinone or Ro-20-1724 enhanced LPS-induced increases in plasma tumor necrosis factor-alpha and lactate, inhibited the LPS-induced tachycardia, and exacerbated the acute LPS-induced fall in GFR. Furthermore, Ro-20-1724-treated rats were unable to maintain MAP. We conclude 1) PDE3 or PDE4 inhibition exacerbates LPS-induced renal failure in conscious rats; and 2) LPS treated rats develop an escape from AVP in the CDs, which could be aimed to protect against water intoxication in septic conditions associated with decreased GFR and high levels of AVP.
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PMID:Lipopolysaccharide-induced acute renal failure in conscious rats: effects of specific phosphodiesterase type 3 and 4 inhibition. 1223 72

In cirrhosis, lipopolysaccharide (LPS, a product of Gram-negative bacteria) in the blood may cause septic shock. LPS-elicited induction of arterial inducible nitric oxide synthase (iNOS) results in nitric oxide (NO)-induced vasodilation, which causes arterial hypotension and hyporeactivity to alpha(1)-adrenergic constrictors. In vitro studies have suggested that vasopressin inhibits iNOS expression in cultured vascular smooth muscle cells exposed to LPS. Thus, the aim of this study was to investigate the effects of terlipressin administration (a vasopressin analog) on in vivo LPS-induced aortic iNOS in rats with cirrhosis. LPS (1 mg/kg, intravenously) was administered followed by the intravenous administration of terlipressin (0.05 mg/kg, intravenously) or placebo 1 hour later. Arterial pressure was measured, and contractions to phenylephrine (an alpha(1)-adrenoceptor agonist), iNOS activity, and iNOS expressions (mRNA and protein) were investigated in isolated aortas. LPS-induced arterial hypotension and aortic hyporeactivity to phenylephrine were abolished in rats that received terlipressin. LPS-induced aortic iNOS activity and expression were suppressed in terlipressin-treated rats. In conclusion, in LPS-challenged rats with cirrhosis, terlipressin administration inhibits in vivo LPS-induced aortic iNOS expression. Terlipressin administration may be a novel approach for the treatment of arterial hypotension and hyporeactivity to alpha(1)-adrenergic constrictors in patients with cirrhosis and septic shock.
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PMID:Terlipressin inhibits in vivo aortic iNOS expression induced by lipopolysaccharide in rats with biliary cirrhosis. 1239 16

Vasopressin secreted by magnocellular neurones of the hypothalamic supraoptic and paraventricular nuclei is essential for water balance. In this study, we examined magnocellular neurone responses to osmotic stimulation in vehicle-injected controls or rats receiving an intraperitoneal (i.p.) injection of 250 microg/100 g of lipopolysaccharide (LPS), 3 h or 6 h earlier. LPS injection had no effect on plasma vasopressin concentrations in control rats but it caused marked and transient potentiation of the responses to a single i.p. injection of hypertonic saline (five- and two-fold, 3 and 6 h after LPS, respectively). The enhancement of plasma vasopressin responses was independent of plasma sodium concentrations or changes in blood pressure. Basal vasopressin mRNA expression in the paraventricular and supraoptic nuclei decreased slightly 6 h after LPS injection, without changes in vasopressin transcription as indicated by vasopressin heteronuclear (hn) RNA levels. Parvocellular neurones showed expected increases in vasopressin hnRNA expression following LPS injection and a further increase after i.p. hypertonic saline injection (due to the painful component). In contrast to magnocellular vasopressin mRNA expression, the effects of LPS and hypertonic saline injections in parvocellular neurones were additive and not synergistic. Light microscopic immunohistochemical examination revealed an increase in size of vasopressin but not oxytocin axonal terminals in the neural lobe 3 h after LPS injection. Osmotic stimulation caused marked depletion of vasopressin immunoreactivity in axonal terminals of the neural lobe in both control and LPS-pretreated rats. The changes in vasopressin axon terminals were accompanied by induction of interleukin (IL)-1 beta and IL-6 in the posterior pituitary. The data show that endotoxemia causes morphological and functional alterations of the hypothalamic neurohypophyseal system, resulting in facilitation rather than inhibition of vasopressin synthesis, and secretion in response to osmotic stimulation.
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PMID:Lipopolysaccharide endotoxin potentiates the effect of osmotic stimulation on vasopressin synthesis and secretion in the rat hypothalamus. 1253 56

This work examines the role of nitric oxide (NO) in the periphery (i.e., on the pituitary) and the brain (particularly on corticotropin-releasing factor [CRF] and vasopressin [VP] neurons in the paraventricular nucleus [PVN] of the hypothalamus) as a modulator of the ACTH response to lipopolysaccharide. We previously showed that NO restricted the pituitary response to VP while it facilitated the synthesis of PVN CRF and VP. In our experience, only relatively high doses of lipopolysaccharide (>50 microg/kg, injected intravenously [i.v.]) cause detectable increases in PVN neuronal activation. Our hypothesis, therefore, was that pituitary NO-VP interactions would predominate in rats injected with a low dose of lipopolysaccharide (0.5 microg/kg, i.v.) while the stimulatory influence of the gas on PVN neuronal activity would play an important role following i.v. injection of a large dose of lipopolysaccharide (50 microg/kg, i.v.). We observed that the ability of 0.5 microg/kg lipopolysaccharide to release ACTH was significantly enhanced by the subcutaneous (s.c.), but not the intracerebroventricular (i.c.v.) injection of L-NAME, an arginine derivative that blocks NO synthesis. The effect of s.c. L-NAME was reversed by immunoneutralization of endogenous VP, which indicated that in this model, the ability of lipopolysaccharide to release ACTH depended, at least in part, on the influence exerted by NO on the pituitary response to VP. In rats injected with the high lipopolysaccharide dose, the s.c. injection of L-NAME decreased plasma ACTH levels compared to those in rats pretreated with the vehicle. The effect of s.c. L-NAME was not significantly altered by VP antibodies. These results indicate that in this model, the primary influence of NO was exerted in the PVN and/or its afferents and that it did not depend on a peripheral, VP-mediated effect of the gas. On the one hand, these data are at odds with our finding that the i.c.v. injection of L-NAME only marginally altered the ACTH response to the large dose of lipopolysaccharide. As i.c.v. injected L-NAME should have primarily decreased hypothalamic, but not pituitary NOS, its only modest influence on ACTH release may have been due to a balance between stimulating and inhibiting effects of NO within the brain. As high doses of lipopolysaccharide increase brain levels of prostaglandin, monoamine, and proinflammatory cytokines, it will be important to investigate the influence exerted by NO on these secretagogues and on their interactions with PVN CRF and VP neurons, which may help us resolve the issues raised by our results. Collectively, these data support our hypothesis that the mechanisms mediating the ACTH response to a low lipopolysaccharide concentration involve the inhibitory VP-mediated influence of NO on pituitary activity. By contrast, the stimulatory effect of high doses of lipopolysaccharide on ACTH release depends, at least in part, on the ability of NO to upregulate PVN neuronal activity.
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PMID:Role of nitric oxide in regulating the rat hypothalamic-pituitary-adrenal axis response to endotoxemia. 1279 48

This study evaluated the role of nitric oxide (NO) in vasopressin (AVP) release induced by intravenous lipopolysaccharide (LPS) in rats previously treated with intracerebroventricular (i.c.v.) saline, L-NAME, L-arginine or sodium nitroprusside (SNP). In control rats given i.c.v. saline, L-NAME, L-arginine or SNP, AVP levels did not change from baseline. After LPS, plasma AVP increased, reaching a peak at 60 min, and returning to basal levels 4 h later in all i.c.v. pre-treated groups (P<0.05). The LPS administration in rats previously treated with L-NAME induced higher AVP levels (P<0.05) that remained elevated throughout the period of the experiment (P<0.05). These findings confirm the inhibitory role of NO in AVP secretion induced by LPS.
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PMID:Role of nitric oxide in lipopolysaccharide-induced release of vasopressin in rats. 1285 May 38

Prostaglandins and histamine in the hypothalamus are involved in the regulation of oxytocin and vasopressin secretion, and appear to be involved in the mediation of pituitary hormone responses to immunochallenges. Therefore, we investigated in conscious male rats: (i) whether blockade of H1 or H2 receptors affected the oxytocin and vasopressin responses to prostaglandins and (ii) whether blockade of prostaglandin synthesis affected the oxytocin and vasopressin responses to histamine or to Escherichia coli lipopolysaccharide (LPS), in order to determine any interaction between prostaglandins and histamine in the hypothalamus. Oxytocin secretion was dose-dependently stimulated by intracerebroventricular infusion of 1 or 5 microg of PGE1, PGE2 or PGF2alpha, with PGE2 being the most potent of the compounds used. Prior central infusion of the H1 receptor antagonist mepyramine or the H2 receptor antagonist cimetidine significantly inhibited the oxytocin response to all three prostaglandins by approximately 50%. Vasopressin secretion was increased by PGE1 but not by PGE2 or PGF2alpha. The stimulatory effect of PGE1 was almost annihilated by prior administration of mepyramine or cimetidine. Central infusion of histamine or immunochallenge with LPS administered intraperitoneally increased oxytocin and vasopressin secretion four- and two-fold, respectively. Pretreatment with systemic injection of the prostaglandin synthesis inhibitor indomethacin dose-dependently reduced the oxytocin response and prevented the vasopressin response to histamine or LPS. We conclude that histamine and PGE1, PGE2 or PGF2alpha interact in the regulation of oxytocin secretion, whereas histamine and only PGE1 interact in the regulation of vasopressin secretion. Furthermore, histamine as well as LPS may affect oxytocin and vasopressin neurones via activation of prostaglandins, probably in the hypothalamic supraoptic nucleus.
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PMID:Histamine and prostaglandin interaction in regulation of oxytocin and vasopressin secretion. 1296 38

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