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)

Interleukin-6 (IL-6) is a proinflammatory cytokine that is normally tightly regulated and expressed at low levels, except during infection, trauma, or other stress. Among several factors that down-regulate IL-6 gene expression are estrogen and testosterone. After menopause or andropause, IL-6 levels are elevated, even in the absence of infection, trauma, or stress. IL-6 is a potent mediator of inflammatory processes, and it has been proposed that the age-associated increase in IL-6 accounts for certain of the phenotypic changes of advanced age, particularly those that resemble chronic inflammatory disease [decreased lean body mass, osteopenia, low-grade anemia, decreased serum albumin and cholesterol, and increased inflammatory proteins such as C-reactive protein (CRP) and serum amyloid A]. Furthermore, the age-associated rise in IL-6 has been linked to lymphoproliferative disorders, multiple myeloma, osteoporosis, and Alzheimer's disease. This overview discusses the data relating IL-6 to age-associated diseases and to frailty. Like the syndrome of inappropriate antidiuretic hormone, it is possible that certain clinically important late-life changes are due to an inappropriate presence of IL-6.
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PMID:Age-associated increased interleukin-6 gene expression, late-life diseases, and frailty. 1077 63

Hypersensitivity reactions to drugs and environmental agents are often due to exaggerated humoral (Th(2)) or cell mediated (Th(1)) immune responses with typical cytokine profiles. Overexpression of Th(2) cytokines, such as IL-4, IL-5 or IL-13 in mice, enhances an IgE antibody mediated response, while deletion of these cytokines attenuates and/or prevents allergic responses. Conversely, modulation of Th(1) cytokine gene expression may affect cell-mediated immune responses. Therefore, cytokine transgenic mice are used as investigative tools to study potential chemicals and/or drug allergies. In addition to cytokines and chemokines, other factors are important for the development of allergic responses, such as IgE, Fc receptors, vasopressin and several other factors, which can be tested in transgenic mice.
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PMID:Use of transgenic animals to investigate drug hypersensitivity. 1116 96

Clinical trials designed to evaluate the effect of drugs and devices on the symptoms and clinical status in chronic heart failure have frequently produced conflicting, inconclusive, or misleading results. These difficulties can be explained by the fact that previous studies have relied on efficacy measures that have inherent limitations and have been analyzed using statistical approaches that ignored episodes of clinical deterioration. Recognition of these pitfalls has led to the development of a new clinical composite score, which combines changes in the New York Heart Association class and the global assessment together with the information provided from the occurrence of major clinical events. Use of this score would have correctly distinguished active therapy from placebo in earlier trials and thus would have avoided some of their misleading conclusions. The new clinical composite score has been prospectively incorporated into the design of studies evaluating the efficacy of endothelin antagonists, cytokine antagonists, vasopressin antagonists, and cardiac resynchronization in the treatment of chronic heart failure. In the trials that have been completed to date, the clinical composite score has been more sensitive than conventional approaches in discerning the presence or absence of a true treatment effect.
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PMID:Proposal for a new clinical end point to evaluate the efficacy of drugs and devices in the treatment of chronic heart failure. 1142 Jul 70

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

Recent studies, which have shown an increase of plasma vasopressin (VP) in experimental motion sickness and the efficacy of VP antagonists for motion sickness, suggest an important role of VP in the development of vestibulo-autonomic responses. We have recently found evidence of the co-existence of vasopressinergic neurons with the stress-sensitive chemokinergic neuronal system in the hypothalamo-pituitary pathway in rats, which uses cytokine-induced neutrophil chemoattractant (CINC) as an effector molecule. In this study, to elucidate possible roles of VP and CINC in the vestibulo-autonomic responses, we simultaneously measured plasma VP and CINC concentrations after electrical or caloric vestibular stimulation in urethane-anesthetized rats. Electrical vestibular stimulation with more than 200 microA increased the plasma levels of VP in a current intensity-dependent manner, and stimulation with 500 microA increased the plasma VP levels to 350% of the normal control group, which received no stimulation. Caloric vestibular stimulation with cold water increased the plasma VP levels to 262% of the control group, which received caloric stimulation with water at 37 degrees C, and stimulation with warm water tended to increase the plasma VP levels. Plasma CINC levels were neither affected by electrical nor caloric vestibular stimulation. These findings indicate that vestibular stimulation increased plasma levels of VP but not CINC, and this vestibular-induced activation of VP neurons may be involved in a mechanism of vestibulo-autonomic responses.
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PMID:Vestibular modulation of plasma vasopressin levels in rats. 1157 10

Following acute or chronic liver tissue damage, hepatic stellate cells (HSCs) undergo a process of activation toward a phenotype characterized by increased proliferation, motility, contractility, and synthesis of extracellular matrix components. Activation of HSCs is regulated by several soluble factors, including growth factors, cytokines, chemokines, and products of oxidative stress, as well as by extensive changes in the composition and organization of the ECM. Different groups of soluble factors may be classified according to their prevalent biological effect: (a) factors promoting HSC proliferation and/or migration (i.e., platelet-derived growth factor, basic fibroblast growth factor, insulin-like growth factor-1); (b) factors promoting fibrillar ECM accumulation, particularly transforming growth factor-beta1; (c) factors with a prevalent contractile effect on HSCs, such as endothelin-1, thrombin, angiotensin-II and vasopressin, although all these agents also may promote HSC proliferation; (d) proinflammatory cytokines and chemokines; and (e) cytokines with a prominent antiinflammatory/antifibrogenic activity, such as interleukin-10 and interferon-gamma. Additional important issues are represented by the relationship between cytokine and integrin signaling, and by the effects of oxidative stress-related molecules on cytokine signaling. In the past decade the major intracellular signaling pathways elicited by these factors in HSCs have been greatly elucidated.
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PMID:Cytokine receptors and signaling in hepatic stellate cells. 1158 68

Chronic heart failure is a complex syndrome involving the activation of multiple cellular, metabolic and neurohumoral pathways following the initial myocardial insult. Because of the complexity of the disease, strategies targeting these multiple systems involved in disease progression are required to maximise the therapeutic benefits of intervention. To this end, there are a number of approaches currently under active evaluation. These include the inhibition of additional neurohormonal vasoconstrictor systems (e.g. endothelin and vasopressin systems), cytokine antagonists (e.g. agents that block tumour necrosis factor-alpha activity), agents that favourably modulate extracellular matrix (e.g. matrix metalloprotease inhibitors) and agents that augment natriuretic peptides.
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PMID:New and emerging pharmacological strategies in the management of chronic heart failure. 1171 86

Magnocellular neurons are innervated by an excitatory histaminergic pathway. They also express neuronal NO synthase, interleukin-1beta (IL-1beta) and cyclo-oxygenase (COX). In normally hydrated rats when NO synthase activity is inhibited with N(G)-nitro-L-arginine methyl ester (L-NAME), administered intracerebroventricularly (i.c.v.), OT concentration in plasma increases. In the present study, the increase in hormone after L-NAME is attenuated by indomethacin, an inhibitor of COX, as well as by antagonists of histamine receptors at H1 (pyrilamine) and H2 (cimetidine) subtypes injected i.c.v. Moreover, enhanced OT secretion induced by centrally administered IL-1beta, but not naloxone (opiate receptor antagonist), is prevented by indomethacin. PGE2 and PGD2 (i.c.v.) stimulate OT release, but only PGD2 affects circulating vasopressin levels. Thus, NO inhibits release of OT stimulated by: (1) a COX-dependent mechanism, i.e. NO-->-(COX-->+PG-->+OT release); (2) histamine, i.e. NO-->-(histamine-->H1 and H2 receptors-->+OT release); and possibly (3) IL-1beta, i.e. NO-->-(IL-1beta-->+COX-->+PG-->+OT release). These interactions of NO, cytokine and histamine may be important for management of stress-induced activation of neuroendocrine systems.
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PMID:Nitric oxide, interleukin and prostaglandin interactions affecting the magnocellular system. 1202 Aug 69

TonEBP is a member of the Rel family of transcriptional activators, distinct from other members NFkappaB and NFAT. In the medulla of mammalian kidney, TonEBP is a local differentiation factor that stimulates the transcription of several genes. The activity of TonEBP is regulated by changes in diuretic status mainly at the level of nucleocytoplasmic distribution. Some of the genes stimulated by TonEBP encode transporters and a synthetic enzyme for cellular accumulation of compatible osmolytes, which protect cells from the deleterious effects of hypertonicity by lowering cellular ionic strength. Other genes include the vasopressin-regulated urea transporters that play a key role in building up high urea concentrations in the renal medulla during antidiuresis and a heat shock protein 70 that protects cells from the deadly effects of urea. TonEBP is also abundantly expressed in other tissues such as brain, heart, liver, and activated T-cells. TonEBP plays a significant role in immunity by stimulating several cytokine genes in the T-cells. A lot more needs to be learned about the genes regulated by TonEBP and signaling pathways from hypertonicity to the activation of TonEBP.
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PMID:TonEBP transcriptional activator in the cellular response to increased osmolality. 1219 10

Heart failure is characterized by sodium and fluid retention, sympathetic overactivity, parasympathetic withdrawal, vasoconstrictor activation and cytokine elevation. New therapies for heart failure attempt to control neurohormonal activation and limit progressive left ventricular dysfunction. Nesiritide (human B-type natriuretic peptide) is a recently approved new vasodilator that has been given to almost 1,000 patients in numerous clinical investigations; it belongs to a new class of heart failure drugs known as natriuretic peptides. Nesiritide decreases pulmonary capillary wedge pressure, systemic vascular resistance, mean right atrial pressure and pulmonary artery pressure, while improving cardiac index, stroke volume and heart failure symptoms. Many endothelin receptor antagonists are in various stages of development. Early clinical studies have demonstrated beneficial cardiovascular hemodynamic effects. Other new drugs for heart failure also include calcium sensitizers, neutral endopeptidase and vasopeptidase inhibitors, aldosterone receptor antagonists, vasopressin antagonists and cytokine inhibitors. All are being actively investigated and many show significant promise as beneficial therapies in the treatment of heart failure.
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PMID:New therapies for the treatment of congestive heart failure. 1253 83


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