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 thick ascending limb of Henle's loop (TAL) is involved in the urinary dilution/concentration process by actively reabsorbing NaCl through a complex mechanism. Some years ago, compelling evidence was provided that cAMP stimulates NaCl reabsorption through the activation of adenylyl cyclase by several hormones other than antidiuretic hormone (ADH). Synthesis of cyclic AMP is inhibited by prostaglandin E2 (PGE2) and arachidonic acid per se, via the pertussis toxin-sensitive protein Gi activation. Cyclic GMP cascade down-regulates NaCl reabsorption, through activation of both guanylyl cyclase receptors (by ANF and urodilatin), and soluble guanylyl cyclase (by nitric oxide, NO). In TAL, NO is produced by the cytokine-inducible form of NO synthase, but not by the constitutive one. Agonists known to activate protein kinase C (PKC) in TAL elicit opposite effects on NaCl reabsorption. Five PKC isoforms belonging to the conventional, novel, and atypical enzyme subclasses have been recently defined in TAL and might differently regulate NaCl flux. Increments in intracellular calcium ([Ca2+]i) inhibit NaCl reabsorption via three pathways: (i) a possible direct effect on ion channels, (ii) a PLA2-mediated production of arachidonic acid derivatives (20-HETE), and (iii) inhibition of the ADH-induced cAMP accumulation. This last effect results from activation of phosphodiesterase (common to the agents that increase [Ca2+]i), and inhibition of adenylyl cyclase (only elicited by Ca2+c). Finally, the apical localization of some agonists effects is documented.
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PMID:Transducing pathways involved in the control of NaCl reabsorption in the thick ascending limb of Henle's loop. 955 29

Although two-way communication between the hypothalamus and the immune system in now well established, particularly for the hypothalamo-pituitary-adrenal axis, the role of the gaseous neurotransmitters nitric oxide (NO) and carbon monoxide (CO) is much less well understood in terms of hypothalamic function. These agents are an important part of the peripheral inflammatory response; and their synthetic enzymes, NO synthase (NOS) and heme oxygenase (HO), respectively, have been localized to the hypothalamic PVN and SON. The induced generation of both NO and CO leads to the suppression of CRH and vasopressin, the major stimulators of the HPA. Thus, the addition of hemin to hypothalamic explants is maximally active at 1 microM in attenuating the release of CRH and vasopressin, and this dose is also most effective in generating biliverdin and associated CO. CO generation is also able to stimulate cyclooxygenase to produce prostaglandin E2, an established intermediary in the cytokine-stimulated activation of the HPA. Finally, inducible NOS mRNA is specifically induced in the hypothalalmus in response to endotoxin, in parallel to interleukin-1. These data provide increasing evidence in favor of NO and CO as counterregulatory agents in the HPA response to immune activation.
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PMID:Acute and subacute effects of endotoxin on hypothalamic gaseous neuromodulators. 962 53

Immune stimulation increases the activity of the HPA axis, a phenomenon directly or indirectly mediated through cytokines. We have used two models, the peripheral administration of endotoxin (LPS) or turpentine-induced tissue injury to show that corticotropin-releasing factor (CRF) and vasopressin (VP), hypothalamic peptides released by cytokines, play a dominant role in the increased ACTH measured in these two paradigms. In turn, CRF and VP synthesis and/or release is modulated by catecholamines, prostaglandins (PGs), and nitric oxide (NO). These secretagogues are produced in the periphery and/or the central nervous system (CNS) in response to increased cytokine levels and act on CRF/VP neurons and nerve terminals. Finally, endotoxemia and local tissue inflammation may upregulate brain levels of tumor necrosis factor alpha, interleukin-1 beta, and/or interleukin-6, providing yet another mechanism through which the occurrence of systemic inflammation is conveyed to the brain. The relative importance of brain or peripheral intermediates appears to depend on the site at which cytokine levels are increased. We have shown, for example, that peripheral, but not brain, PGs are important in mediating the neuroendocrine influence of blood-borne cytokines, while PGs in the CNS play a role in situations characterized by elevated brain immune proteins. NO, on the other hand, restrains the response of the HPA axis to circulating, but not brain cytokines. These results illustrate the complexity of the mechanisms involved in the stimulation of the HPA axis and suggest that their specific involvement depends on the type, intensity, and duration of immune stimulation.
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PMID:Mechanisms of hypothalamic-pituitary-adrenal axis stimulation by immune signals in the adult rat. 962 70

The authors evaluated the relationship between hormonal and cytokine responses after surgery. Patients who underwent thoracic oesophagectomy (O group; n = 7), pulmonary lobectomy (P group; n = 5), modified mastectomy (M group; n = 5) and laparoscopic cholecystectomy (LC group; n = 7), were randomly selected. Circulating neutrophil and lymphocyte numbers were assayed. Changes in the concentration of the hormones [adrenocorticotrophic hormone (ACTH), cortisol, and antidiuretic hormone (ADH)] and cytokines [tumour necrosis factor alpha (TNF-alpha), interleukin 1 beta (IL-1 beta), IL-6, and IL-10] were analysed. In O and P groups, neutrophils were still seen on post-operative day (POD) 3, while the leukocyte counts of M and LC groups returned to normal. The number of lymphocytes significantly decreased on POD1 and POD3 only after oesophagectomy. The pattern of hormonal levels was consistent in all groups. While TNF-alpha and IL-1 beta were undetectable in the peripheral blood, the concentration of IL-6 and IL-10 increased in O and P groups, but not in M and LC groups. The degree of lymphocytepenia and neutrophilia correlated well with the extent of surgical trauma.
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PMID:Changes in immune-endocrine response after surgery. 970 20

In the rat, the acute administration of alcohol induces dose-related increases in plasma ACTH and corticosterone levels. This response depends on the delivery of the hypothalamic peptides corticotropin-releasing factor and vasopressin (VP) to the pituitary. On the other hand, exposure to an alcohol diet for 7 to 10 days significantly blunts the hypothalamic-pituitary-adrenal (HPA) axis in response to other homeostatic threats, such as mild electroshocks or immune signals. This decreased response is at least in part due to an attenuated ability of VP to increase ACTH secretion. We have previously shown that nitric oxide (NO) inhibits the pituitary response to VP. We therefore hypothesized that chronic alcohol treatment might increase levels of this gas within the HPA axis, and tested this possibility by determining whether blockade of NO formation might restore a normal pituitary response to VP. We observed that such was the case, and therefore propose that NO participates in the blunted activity of the HPA axis during prolonged exposure to alcohol. Finally, we determined whether alcohol would exert neuroendocrine effects that extended beyond the initial drug treatment. To explore this possibility, we injected rats with alcohol intragastrically for 3 days, then re-exposed them to the drug 3 to 12 days later. Rats pretreated with the vehicle and injected with alcohol several days later showed the expected significant rise in plasma ACTH and corticosterone levels, as well as a marked increase in immediate early genes mRNA levels in the paraventricular nucleus (PVN) of their hypothalamus. In contrast, animals pretreated with alcohol exhibited a blunted hormonal and hypothalamic response during the second drug exposure but, interestingly, retained a normal endocrine response to other signals, such as exposure to electro-footshocks or cytokine injection. We originally thought that this phenomenon of selective endocrine tolerance might be explained by decreased serotonin levels in the PVN. Whereas alcohol indeed decreased concentrations of this neurotransmitter in the PVN, exposure to electroshocks induced similar changes. However, an initial exposure to shocks did not blunt the ability of the HPA axis to be activated by a second shock session, by alcohol or by immune signals (delivered several days later). These results do not support the hypothesis that the decreased HPA axis response to a second alcohol challenge is mediated via decreased serotonin afferents to corticotropin-releasing factor neurons in the PVN.
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PMID:Mechanisms mediating the influence of alcohol on the hypothalamic-pituitary-adrenal axis responses to immune and nonimmune signals. 972 44

The role played by nitric oxide (NO) and carbon monoxide (CO) was explored in the adult male rat by determining whether antagonizing the activity of the enzymes responsible for the formation of these gases altered the response of the hypothalamic-pituitary-adrenal (HPA) axis to immune (cytokines) or nonimmune (mild electroshocks) signals. The arginine derivative Nomeganitro-L-arginine-methylester (L-NAME), which inhibits all three NO synthase (NOS) isoforms [inducible (i), endothelial (e) and neuronal (n)] significantly augments the ACTH response to blood-borne cytokines, but decreases it in rats exposed to shocks or other physico-emotional stresses. The effect of L-NAME in both models is mimicked by L-nitroarginine (L-NNA) and L-nitromethylarginine (L-NMMA), which block constitutive (e and n) forms of NOS, but not by aminoguanidine (which blocks iNOS) or 7-nitroindazole (which specifically blocks nNOS). Despite the ability of L-NAME to markedly augment the stimulatory effect of vasopressin on ACTH secretion, removal of this peptide does not interfere with the interaction between L-NAME and systemically administered interleukin-1beta (IL-1beta). In contrast, blockade of prostaglandin formation prevents both the stimulatory effect of IL-1beta on ACTH release, and its potentiation by L-NAME. In contrast to the investigation of the importance of endogenous NO, studies focused on the role of CO remain scarce. Our preliminary results suggest that while blockade of the formation of this gas decreases the ACTH response to various stimuli, it also significantly interferes with the effect of L-NAME in rats systemically administered cytokines, and further decreases the ACTH response to shocks in animals also injected with arginine analogs. These results indicate the possible presence of functional interactions between NO and CO in regulating the activity of the HPA axis. Our present working hypothesis is that in the presence of elevated circulating cytokine levels, endogenous NO acts presynaptically to inhibit the release of ACTH secretagogues from nerve terminals in the infundibulum. As the acute ACTH response to these immune proteins is believed to primarily depend on events taking place within the median eminence, blockade of NO formation results in exaggerated ACTH release. During exposure to shocks and other nonimmune stresses, on the other hand, increased ACTH secretion is primarily due to activation of hypothalamic neurons. In this case, because of the stimulatory influence of endogenous NO on hypothalamic perikarya that manufacture corticotropin-releasing factor (CRF) and/or of the afferents to these neurons, blockade of NOS activity blunts CRF production, and consequently ACTH release. What remains undetermined is the net effect of the opposite influences of NO during long-term exposure to immune or nonimmune stress. Finally, it is possible that the conflicting results reported by investigators who study the role of NO and CO in isolated cell preparations may reflect, at least in part, these opposite effects of NO on different elements of the HPA axis.
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PMID:Role of nitric oxide and carbon monoxide in modulating the ACTH response to immune and nonimmune signals. 973 Jun 87

Interferons (IFNs) are now in use worldwide for the treatment of chronic viral hepatitis. Unfortunately, various side effects of IFNs have been reported. Because cytokines, which include IFNs, can affect endocrine function, endocrinological abnormalities are sometimes observed in patients treated with IFNs. We examined the effects of IFN-beta on peripheral levels of pituitary and adrenal hormones and cytokines. Six million international units of IFN-beta dissolved in glucose solution was injected for 30 min. As a control study, glucose solution without IFN-beta was injected. Pituitary hormones (ACTH, GH, TSH, prolactin (PRL), LH, FSH, and arginine-vasopressin (AVP)), cortisol, and cytokines such as interleukin (IL)-1, IL-6, tumor necrosis factor-alpha (TNF), and interleukin-1 receptor antagonist (IL-1ra) were measured before and after IFN-beta injection. The study was carried out on 14 patients with chronic hepatitis type C who were under treatment with IFN-beta. All studies were performed when the patients were afebrile. None of the patients had any endocrine or autoimmune diseases. Plasma ACTH levels increased significantly at 60-120 min after IFN-beta injection compared with the levels before IFN-beta injection and in the control study using glucose injection. Plasma cortisol levels increased after IFN-beta injection, in parallel with plasma ACTH elevation. Serum GH levels increased significantly at 120 min after IFN-beta injection. All the increased hormones including ACTH, cortisol, and GH, were decreased at the end of the study-180 min after IFN-beta injection. Serum levels of TSH, PRL, LH, FSH, and AVP were not changed significantly by IFN-beta injection. Plasma IL-1 and TNF levels did not change after IFN-beta injection, while IL-6 and IL-1ra were elevated significantly. The increases in IL-6 and IL-1ra were gradual, reaching their peak levels at 180 min after IFN-beta injection. However there were no correlations between the hormones measured in this study and the levels of IL-6 or IL-1ra. It would seem that IFN-beta has direct or indirect stimulatory effects for ACTH and GH without mediation of the cytokines. These in vivo results are important for investigating the relationship between endocrine and cytokine systems in humans.
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PMID:Change of peripheral levels of pituitary hormones and cytokines after injection of interferon (IFN)-beta in patients with chronic hepatitis C. 976 84

It is now largely established that the immune and neuroendocrine systems cross-talk by using similar ligands and receptors. In this context, the thymus-hypothalamus/pituitary axis can be regarded as a paradigm of connectivity in both normal and pathological conditions. For example, cytokines and thymic hormones modulate hypothalamic-pituitary functions: (a) interleukin (IL)-1 seems to upregulate the production of corticotropin-releasing factor and by adrenocorticotropin by hypothalamic neurons and pituitary cells, respectively; (b) thymulin enhances LH secretion. Conversely, a great deal of data strongly indicate that the hypothalamic-pituitary axis plays a role in the control of thymus physiology. Growth hormone (GH) for example, enhances thymulin secretion by thymic epithelial cells (TEC), both in vivo and in vitro, also increasing extracellular matrix-mediated TEC/thymocyte interactions. Additionally, gap junction-mediated cell coupling among TEC is upregulated by ACTH. In a second vein, it was shown that GH injections in aging mice increased total thymocyte numbers and the percentage of CD3-bearing cells, as well concanavalin-A mitogenic response and IL-6 production. In addition to mutual effects, thymus-pituitary similarities for cytokine and hormone production have been demonstrated. Cytokines such as IL-1, IL-2, IL-6, interferon-gamma, transforming growth factor-beta and others can be produced by hypothalamic and/or pituitary cells. Conversely, hormones including GH, PRL, LH, oxytocin, vasopressin and somatostatin can be produced intrathymically. Moreover, receptors for various cytokines and hormones are expressed in both the thymus and the hypothalamus/pituitary axis. Lastly, it is noteworthy that a thymus-pituitary connectivity can also be seen under pathological situations. In this regard, an altered HPA axis has been reported in AIDS, human falciparum malaria and murine rabies, that also show a severe thymic atrophy.
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PMID:Immunoneuroendocrine connectivity: the paradigm of the thymus-hypothalamus/pituitary axis. 987 43

Interleukin-6 (IL-6) is an important mediator of the acute phase response and a sensitive marker of tissue damage. This study was conducted to investigate the fluctuation of serum cytokine and hormonal levels during the perioperative period after laparoscopic-assisted colectomy (LAC), and the data were compared with those after conventional open colectomy (OPEN). The subjects comprised eight patients who underwent OPEN and eight who underwent LAC. Blood samples were obtained by peripheral vein puncture before the induction of anesthesia, then 2, 4, 6, 8, 24, 48, and 72 h after skin incision to measure the levels of serum IL-6, adrenocorticotropic hormone (ACTH), cortisol, and antidiuretic hormone (ADH). The level of serum IL-6 increased significantly during the perioperative course in both groups; however, the level 4 h after the commencement of surgery and the peak level were significantly lower in the LAC group than in the OPEN group (P < 0.05). Plasma ACTH, cortisol, and ADH rapidly increased in both groups, but there was no significant difference between them. The IL-6 levels in collected ascites samples were not significantly different between the two groups. The changes in serum IL-6 levels indicate that LAC is less invasive than conventional open colectomy. These findings corresponded well with the clinical courses of the patients who underwent the two types of operations.
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PMID:Cytokine and hormonal responses in laparoscopic-assisted colectomy and conventional open colectomy. 1066 30

In previous study of melanocyte-stimulating hormone (MSH) cell development in the proliferating pars intermedia, which is in close apposition to the presumptive pars nervosa, no direct cell-to-cell contact was found between the boundary neurohypophyseal pituicytes (PIC), adenohypophyseal precursor stem cells (PSC) and the related diencephalic mesenchymal cells. Here, we have used immunohistochemistry to examine cytokine expression in the development of the hypophysis during foetal stages II-IV. Light and confocal laser scanning microscopy indicated diffuse expression of both TGF alpha and EGF in the hypophysis at different foetal stages. While no findings indicative for temporary changes of TGF alpha and EGF patterns were found in the foetal hypophysis, a temporary increment of EGF molecules was distinct in the diencephalic mesenchyme at stages III and IV. On the other hand, light microscopy intensively immuno-localized EGFR in the adenohypophysis and neurohypophysis at different developmental stages. Immunoreactivity of EGFR in the cytoplasm and nucleus suggested active proliferative events in the PIC and PSC of stages II-IV mouse pituitaries.
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PMID:Immunohistochemical localisation of epidermal growth factor, transforming growth factor alpha and EGF receptor during organogenesis of the murine hypophysis in vivo. 1077 27


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