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 usefulness of arteriography and transcatheter treatment was studied in nine patients with gastrointestinal hemorrhage and acquired immunodeficiency syndrome (AIDS). Selective arteriography was performed in all patients; transcatheter treatment was performed by means of embolotherapy or selective vasopressin infusion. Medical records were reviewed to determine the cause of hemorrhage and clinical outcome. Arteriography enabled identification of the site of hemorrhage in seven patients. Hemorrhage was caused by Kaposi sarcoma (n = 2), cytomegalovirus colitis (n = 1), lymphoma (n = 2), or unknown causes (n = 4). Neovascularity and dense parenchymal stain were present in patients with Kaposi sarcoma. Transcatheter treatment consisted of embolization (n = 3), vasopressin infusion (n = 2), or both (n = 1). Hemorrhage was controlled in six cases in which transcatheter treatment was administered. Complications included thrombosis of the femoral artery in a 7-month-old infant and formation of a pseudoaneurysm of the femoral artery, which was treated successfully with ultrasound-guided compression. In patients with AIDS and profuse gastrointestinal hemorrhage, arteriography often enables identification of a specific site of hemorrhage, which can be stopped with transcatheter treatment.
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PMID:Gastrointestinal hemorrhage in AIDS: arteriographic diagnosis and transcatheter treatment. 141 Mar 52

The causes and management of endocrine disorders associated with human immunodeficiency virus (HIV) infection are reviewed. Endocrine disorders observed in HIV-positive patients include adrenal abnormalities, hyporeninemic hypoaldosteronism, pituitary insufficiency, pancreatic abnormalities, thyroid and parathyroid disorders, and testicular abnormalities. Opportunistic pathogens implicated in these disorders include cytomegalovirus, Cryptococcus, Toxoplasma, mycobacteria, Candida, and Aspergillus. Neoplasma such as Kaposi's sarcoma and lymphoma can also cause endocrine abnormalities. Several drugs used in patients with the acquired immunodeficiency syndrome (AIDS) are associated with the development of endocrine disorders. These drugs include ketoconazole, itraconazole, rifampin, vidarabine, pentamidine, trimethoprim-sulfamethoxazole, didanosine, and ganciclovir. Severe patient debilitation can contribute to the development of endocrine abnormalities. Monitoring of adrenal gland function may be prudent in HIV-infected patients who have nonspecific symptoms of adrenal insufficiency. If adrenal insufficiency is diagnosed, replacement therapy with oral hydrocortisone is required. Administration of fludrocortisone can rapidly alleviate the signs and symptoms of hyporeninemic hypoaldosteronism. Fluid restriction is the first step in managing the pituitary abnormality known as the syndrome of inappropriate secretion of antidiuretic hormone. Drug-induced endocrine abnormalities often resolve after withdrawal of the offending agent. Endocrine complications in HIV-infected patients may be caused by infection, malignancy, or drugs. Adjusting or instituting drug therapy may be necessary to control symptomatic endocrine abnormalities.
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PMID:Endocrine complications associated with human immunodeficiency virus infection. 151 43

The aquaporins (AQPs) are a family of homologous water-channel proteins that can be inserted into epithelial cell plasma membranes either constitutively (AQP1) or by regulated exocytosis following vasopressin stimulation (AQP2). LLC-PK1 porcine renal epithelial cells were stably transfected with cDNA encoding AQP2 (tagged with a C-terminal c-Myc epitope) or rat kidney AQP1 cDNA in an expression vector containing a cytomegalovirus promoter. Immunofluorescence staining revealed that AQP1 was mainly localized to the plasma membrane, whereas AQP2 was predominantly located on intracellular vesicles. After treatment with vasopressin or forskolin for 10 min, AQP2 was relocated to the plasma membrane, indicating that this relocation was induced by cAMP. The location of AQP1 did not change. The basal water permeability of AQP1-transfected cells was 2-fold greater than that of nontransfected cells, whereas the permeability of AQP2-transfected cells increased significantly only after vasopressin treatment. Endocytotic uptake of fluorescein isothiocyanate-coupled dextran was stimulated 6-fold by vasopressin in AQP2-transfected cells but was only slightly increased in wild-type or AQP1-transfected cells. This vasopressin-induced endocytosis was inhibited in low-K+ medium, which selectively affects clathrin-mediated endocytosis. These water channel-transfected cells represent an in vitro system that will allow the detailed dissection of mechanisms involved in the processing, targeting, and trafficking of proteins via constitutive versus regulated intracellular transport pathways.
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PMID:Constitutive and regulated membrane expression of aquaporin 1 and aquaporin 2 water channels in stably transfected LLC-PK1 epithelial cells. 754 77

The free calcium concentrations in the nucleus ([Ca2+]n) and in cytosol ([Ca2+]c) of cultured human embryonic lung (HEL) fibroblasts were estimated by confocal laser microscopy using the Ca(2+)-indicator Indo-1. In resting HEL cells, The free cellular Ca(2+)-concentration significantly increased upon human cytomegalovirus (HCMV) infection. The ratio between [Ca2+]n and [Ca2+]c was not affected. Following stimulation by ATP or [Arg8] vasopressin (AVP), a differential Ca2+ response of the HCMV-infected HEL cells was observed. While uninfected cells were highly sensitive to AVP and only poorly sensitive to ATP, infected cells showed a high responsiveness to ATP but not to AVP. This switch in sensitivity to the agonists first observed at 24 h post infection. The Ca(2+)-rise following ATP or AVP stimulation was derived from intracellular Ca2+ stores. The magnitude of the ATP-induced Ca(2+)-rise increased upon infection. In contrast to non-infected cells where [Ca2+]n > [Ca2+]c during stimulation with AVP or ATP, no nucleo-cytosolic Ca(2+)-gradient was observed in infected cells. Furthermore, the magnitude of the Ca2+ rise in the two compartments was higher in ATP-stimulated cells. It is concluded that HCMV infection significantly interferes with Ca(2+)-homeostasis in HEL cells which could be related to the pathogenesis of the disease.
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PMID:Human cytomegalovirus modulates the Ca2+ response to vasopressin and ATP in fibroblast cultures. 758 88

We report an autopsy case of granulomatous angiitis of the central nervous system (GANS) complicated by the syndrome of inappropriate antidiuretic hormone (SIADH). A 88-year old female was admitted because of progressive mental deterioration, fever, and vomiting. A computed tomogram disclosed bilateral periventricular lucency, and a low-density area in the right occipital lobe. Laboratory studies during her hospital stay, revealed hyponatremia, hypoalbuminemia, and increased antidiuretic hormone. Treatment with antibiotics, hypertonic saline solution, and steroids, and water restriction was ineffective, and the patient died six weeks after admission. Autopsy examination of the brain revealed slightly turbid meninges with multiple small infarctions in the corona raiata of both cerebral hemispheres. Microscopic study disclosed granulomatous inflammation with many giant cells in the walls of small and medium sized vessels, and the adventitia and media were more involved than the intima. Their lumens were narrowed, and many thrombi were observed. Extensive non-granulomatous inflammatory change was found mainly in the subarachnoid space. All of these findings were similar to the GANS firstly reported by Cravioto et al, in 1959. Since the blood vessels in the central nervous system play an important part in any inflammatory conditions and the blood vessels may be involved by bacterial, fungal, parasitic or viral meningitis, various microorganisms have been suspected as the cause of GANS, including mycoplasma, herpes zoster, herpes simplex viruses, cytomegalovirus, and human T-lymphotropic virus type III (HTLV-III). Some reported cases have been associated with Hodgkin's disease and cerebral amyloid angiopathy. We could not identify any cause in our case.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Granulomatous angiitis of the central nervous system complicated by the syndrome of inappropriate antidiuretic hormone]. 760 90

1. Cytomegalovirus (CMV) is a major pathogen in immunocompromised individuals and may participate in the pathogenesis of atherosclerosis in the general population. We evaluated whether CMV-infection alters the function of arterial smooth muscle. 2. Blood pressure (BP) and arterial reactivity were recorded in immunosuppressed rats that had been infected with CMV (10(5) plaque forming units i.p.). Furthermore, the reactivity of isolated arteries was compared between CMV-infected rats and rats injected with bacterial endotoxin (LPS). 3. Initially resting BP and heart rate (HR) were not modified in CMV-infected rats, but baroreflex control of HR was impaired. By the eighth day post-CMV, BP dropped precipitously and could no longer be raised by phenylephrine (PHE). 4. In mesenteric resistance arteries, isolated at this stage from CMV-infected rats, contractile responses to nerve stimulation, noradrenaline, PHE and 5-hydroxytryptamine (5-HT) were virtually absent while those to high potassium and vasopressin (AVP) were not modified. In aortae of CMV-infected rats, responses to 5-HT and AVP were impaired while those to PHE or potassium were hardly affected. Reduced contractile responses could not be restored by NG-nitro-L-arginine methyl ester (L-NAME). 5. Continuous treatment of CMV-infected rats with prazosin (0.1 mg kg-1 day-1) prevented blood pressure lowering and resistance artery changes. 6. Observations in arteries of LPS-treated rats (5-10 mg kg-1, i.p.) differed markedly from those in vessels of CMV-infected animals. The contractile reactivity of their mesenteric resistance arteries was not altered while in their aortae, responses to PHE, 5-HT and AVP were reduced. With the exception of the AVP responses, this was more pronounced in the presence of 1-arginine and reversed by L-NAME. 7. These findings indicate that CMV-infection results in a reduction of resistance artery reactivity and hypotonia. This seems not to involve cytokine-mediated induction of NO synthase in the vascular wall but may be due to alterations of excitation-contraction coupling in arterial smooth muscle in response to increased sympathetic nervous input.
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PMID:Impaired arterial reactivity following cytomegalovirus infection in the immunosuppressed rat. 890 36

Transcripts encoding the vasopressin precursor are located in axons and dendrites of rat hypothalamic magnocellular neurons. While the axonal vasopressin mRNA has been extensively characterized both at the biochemical and morphological level, little is known about those transcripts residing in dendrites of magnocellular neurons. As revealed by in situ hybridization at the electron microscopic level, the mRNA is located in proximal and distal dendritic segments and is exclusively confined to regions containing rough endoplasmic reticulum. These results suggest that dendrites of hypothalamic neurons may be capable of local precursor synthesis independent of that occurring in the cell somata. A heterologous system has been employed to define cis-acting elements within the vasopressin mRNA which may be involved in dendritic compartmentalization. Expression vector constructs consisting of the cytomegalovirus promoter coupled to the rat vasopressin cDNA have been injected into the cell nuclei of cultured neurons derived from embryonic rat superior cervical ganglia. Vector-encoded vasopressin transcripts were also sorted to dendrites of these neurons indicating that the molecular determinants of dendritic mRNA transport are not cell specific. Mapping of the targeting elements revealed two segments within the vasopressin mRNA that are able to confer dendritic compartmentalization to alpha-tubulin mRNA which is normally confined to the cell body.
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PMID:Dendritic localization of rat vasopressin mRNA: ultrastructural analysis and mapping of targeting elements. 910 94

In patients with acquired immune deficiency syndrome (AIDS), hypoosmolality is frequently observed, whereas hypernatremia is distinctly rare. We report two patients with advanced AIDS and cytomegalovirus (CMV) encephalitis, who developed severe hypernatremia without any thirst sensation, that is, adipsic hypernatremia. Both developed severe hypernatremia of up to 164 and 162 mmol/L, with serum osmolalities of 358 and 344 mOsmol/kg while remaining alert and denying thirst. Serum antidiuretic hormone (ADH) levels were 0.9 and 1.5 pg/mL, inappropriately low for the concomitant serum osmolalities. Vital signs were stable. During hypernatremia, urine osmolalities were 327 and 340 mOsmol/kg, and urine Na+ levels were 56 and 119 mmol/L, respectively. Periventricular white matter lesions were seen on cerebral nuclear magnetic resonance imaging (NMRI) in case 1, but the pituitary appeared normal in both cases. Survival after onset of hypernatremia was 6 and 4 weeks, respectively. Autopsy in case 1 showed typical findings of CMV encephalitis but normal pituitary, confirming that infection with HIV or CMV most likely caused the dysfunction of the central osmostat.
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PMID:Adipsic hypernatremia in two patients with AIDS and cytomegalovirus encephalitis. 1002 54

The possibility of the brain-specific expression of a component of the renin-angiotensin system was evaluated in the present study. We used the hemagglutinating virus of Japan-liposome complex to transfect human angiotensin-converting enzyme (ACE) cDNA, driven by the cytomegalovirus enhancer and beta-actin promoter, into the lateral cerebroventricle of male Sprague-Dawley rats. We evaluated the time course of hemodynamics, the tissue levels of angiotensin (Ang) II and vasopressin, and ACE activity. Intracerebroventricular transfection of the human ACE gene increased both blood pressure and heart rate. Transfected rats exhibited higher concentrations of brain Ang II and increased brain ACE activity. This activation of the brain angiotensin system was accompanied by increased vasopressin production. The increases in blood pressure and heart rate were abolished by intracerebroventricular administration of an ACE inhibitor or Ang II type 1 receptor antagonist. The expression of the transgene was widely distributed in the periventricular cell layer, the cortex, the hypothalamic nuclei, and the brain stem. Expression in the neuronal cells persisted for up to 14 days. Thus, this hemagglutinating virus of Japan-liposome method is a highly efficient system for gene delivery and is extremely useful for functional gene transfection. This novel hypertensive model may enable characterization of the functions of the renin-angiotensin system in the brain and determination of its role in the pathogenesis of hypertension.
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PMID:Activation of the brain angiotensin system by in vivo human angiotensin-converting enzyme gene transfer in rats. 1045 58

A case of angiotropic B-cell lymphoma associated with hemophagocytic syndrome (HPS) has been reported. In addition to fever, pancytopenia, hepatosplenomegaly, and lack of lymphadenopathy, unique clinical features, such as syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and pulmonary infarction, were manifested. Both soluble interleukin-2 receptor (sIL-2R) and IL-6 were elevated in the patient's sera in addition to an increase of serum lactate dehydrogenase and ferritin. In contrast, tumor necrosis factor-alpha and interferon-gamma were within normal ranges. Serum antibodies against Epstein-Barr virus and cytomegalovirus showed a past infection pattern. An autopsy examination revealed systemic intravascular proliferation of lymphoma cells with a B-cell phenotype, confirming the diagnosis of angiotropic B-cell lymphoma. Moreover, SIADH was suggested to result from the infiltration of tumor cells into the pituitary gland. Triple association of angiotropic B-cell lymphoma, HPS and SIADH is quite rare. Therefore, the present case seems to be helpful for clarifying the mechanism for HPS of non-Hodgkin's lymphoma with B-cell origin.
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PMID:Angiotropic B-cell lymphoma with hemophagocytic syndrome associated with syndrome of inappropriate secretion of antidiuretic hormone. 1110 Jul 51


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