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)

The influence of exogenous endotoxin pretreatment on liver regeneration after partial hepatectomy was evaluated. Partial hepatectomy was performed by 67% liver resection of ether-anesthetized rats with midline laparotomy and liver manipulation as the sham control. Animals were pretreated with endotoxin at a dose of 33 micrograms/100 g sc or iv 24 h before surgery and then fasted. Liver regeneration was quantified after partial hepatectomy by [3H]thymidine incorporation into hepatic DNA, and plasma levels of hepatotrophic factors were measured by radioimmunoassay or radioreceptor assay. Systemic endotoxemia occurred after exogenous endotoxin administration as well as after partial hepatectomy due to absorption of exogenous endotoxin from the gut into the portal circulation as determined by quantitative chromogenic lysate assay of perchloric acid-extracted plasma samples. Alterations in putative hepatotrophic factors, including insulin, glucagon, epidermal growth factor, vasopressin, and triiodothyronine, were remarkable similar in response to endotoxemia by exogenous endotoxin administration and by endogenous endotoxin absorption from the gut after partial hepatectomy. Our hypothesis purports that gut-derived systemic endotoxemia elicits hepatotrophic factor secretion for liver regeneration after partial hepatectomy and that endotoxin pretreatment expedites the hepatotrophic factor response, thus accelerating DNA synthesis in the proliferating liver after 67% resection.
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PMID:Gut-derived endotoxin elicits hepatotrophic factor secretion for liver regeneration. 286 2

Liver regeneration following partial hepatectomy is significantly impaired in rats with hereditary vasopressin deficiency (Brattleboro strain), both in rate of DNA synthesis and in return of liver DNA content to normal. Vasopressin treatment at physiological doses ameliorates the defect and thus appears to be an important modulator of liver regeneration in response to partial hepatectomy in the rat.
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PMID:Vasopressin modulates liver regeneration in the Brattleboro rat. 688 53

Liver regeneration following partial hepatectomy is significantly impaired in rats with hereditary vasopressin (AVP) deficiency. This suggested that AVP might have a direct effect on cultured rat hepatocytes. Hepatocytes from male Sprague-Dawley rats were isolated using a two-step collagenase perfusion technique and plated at a density of 10(5)/16-mm Primaria plate. After a suitable attachment period, hepatocytes were incubated with minimal essential media, AVP, AVP plus a specific AVP antagonist, or oxytocin. Hepatocyte proliferation was measured by [3H]thymidine incorporation ([3H]Thy) into hepatocyte DNA. AVP (10 nM) increased [3H]Thy significantly (and this effect was blocked by an AVP-specific antagonist (50 nM). Oxytocin had no effect on hepatocyte DNA synthesis. To further investigate the influence of AVP on hepatocyte proliferation, the effect of AVP on transforming growth factor-alpha (TGF-alpha)-stimulated hepatocyte proliferation was also studied. This combination was chosen based on the ability of AVP to inhibit the biologic effects of EGF (a TGF-alpha analog). There was significant attenuation of TGF-alpha (50 nM)-stimulated [3H]Thy in the presence of AVP (10 nM). In summary: (1) AVP stimulates proliferation of cultured rat hepatocytes. (2) The effect of AVP can be significantly abolished by a specific AVP antagonist. (3) The proliferative response of AVP is specific. (4) AVP significantly attenuates TGF-alpha-stimulated hepatocyte hepatic DNA synthesis. Further studies should elucidate the mechanisms for the effects of AVP on hepatic proliferation alone or in combination with other factors.
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PMID:Vasopressin stimulates DNA synthesis in cultured rat hepatocytes. 799 50

Liver regeneration is significantly impaired in rats with both alpha-adrenergic hepatic denervation and hereditary vasopressin deficiency. This may implicate a direct role for these agonists in the process of compensatory hyperplasia. The mitogenic capacities of norepinephrine, vasopressin and hepatocyte growth factor (HGF), either alone or in combination were investigated by [3H]thymidine incorporation into hepatocyte cultures prepared from normal and regenerating rat livers. The results show that normal hepatocytes incorporate less [3H]thymidine in response to HGF than do regenerating hepatocytes. In addition, physiological concentrations of vasopressin cause a synergistic stimulation of [3H]thymidine uptake in rat liver cells in the presence of HGF.
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PMID:Vasopressin synergistically stimulates DNA synthesis in normal and regenerating rat liver cell cultures in the presence of hepatocyte growth factor. 913 2

Liver regeneration after partial hepatectomy is a plastic process during which the mechanisms that coordinate liver mass restoration compensate one another through a complex regulatory network of cytokines, growth factors, and hormones. Vasopressin, an agonist that triggers highly organized Ca2+ signals in the liver, may be one of these factors, although little in vivo evidence is available in support of this hypothesis. We provide evidence that hypothalamic vasopressin secretion is stimulated early after partial hepatectomy. Although hepatocytes were fully responsive to vasopressin during the first hours of regeneration, they became desensitized and exhibited slow oscillating Ca2+ responses to vasopressin on the following days. On the first day, hepatocyte V1a receptor density decreased and its lobular gradient increased in hepatectomized rats. By antagonizing the V1a receptor in vivo, we demonstrated that vasopressin contributes to NF-kappaB and cyclin (D1 and A) activation, to hepatocyte progression in the cell cycle, and to liver mass restoration. Finally, vasopressin exerted a choleretic effect shortly after hepatectomy, both in the isolated perfused liver and in the intact rat. In conclusion, we provide compelling in vivo evidence that vasopressin contributes significantly to growth initiation and bile flow stimulation in the early stages of liver regeneration.
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PMID:Hypothalamic vasopressin release and hepatocyte Ca2+ signaling during liver regeneration: an interplay stimulating liver growth and bile flow. 1451 67