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)

In the search for a more potent bombesin antagonist, we found [D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P to be effective in mouse fibroblasts and to inhibit the growth of small cell lung cancer, a tumor that secretes bombesin-like peptides that may act as autocrine growth factors. In murine Swiss 3T3 cells, [D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P proved to be a bombesin antagonist as judged by the following criteria: (i) inhibition of DNA synthesis induced by gastrin-releasing peptide and other bombesin-like peptides; (ii) inhibition of 125I-labeled gastrin-releasing peptide binding to the bombesin/gastrin-releasing peptide receptor; (iii) reduction in cross-linking of the Mr 75,000-85,000 protein putatively a component of the bombesin/gastrin-releasing peptide receptor; (iv) blocking of early cellular events that precede mitogenesis--calcium mobilization and inhibition of epidermal growth factor binding. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P was 5-fold more potent than the antagonist [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P. [D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P also inhibits mitogenesis induced by vasopressin but not that induced by a variety of other mitogens. Both antagonists reversibly inhibited the growth of small cell lung cancer in vitro in a concentration-dependent manner. Peptide antagonists could, therefore, have far-reaching therapeutic implications.
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PMID:[D-Arg1,D-Phe5,D-Trp7,9,Leu11]substance P, a potent bombesin antagonist in murine Swiss 3T3 cells, inhibits the growth of human small cell lung cancer cells in vitro. 245 Mar 49

We have shown previously that pp60c-src is a substrate for protein kinase C in vivo and that the target of protein kinase C phosphorylation in mammalian pp60c-src is serine 12. We now demonstrate that in addition to tumor promoters, all activators of phosphatidylinositol turnover that we have tested in fibroblasts (platelet-derived growth factor, fibroblast growth factor, serum, vasopressin, sodium orthovanadate, and prostaglandin F2 alpha) lead to the phosphorylation of pp60c-src at serine 12. In addition to stimulating serine 12 phosphorylation in pp60c-src, platelet-derived growth factor treatment of quiescent fibroblasts induces phosphorylation of one or two additional serine residues and one tyrosine residue within the N-terminal 16 kilodaltons of the enzyme and activates its immune complex protein-tyrosine kinase activity.
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PMID:Platelet-derived growth factor induces multisite phosphorylation of pp60c-src and increases its protein-tyrosine kinase activity. 246 76

New fluorescent Na+ indicators, SBFI (short for sodium-binding benzofuran isophthalate) and SBFP (short for sodium-binding benzofuran phthalate) (Minta, A., and Tsien, R. Y. (1989) J. Biol. Chem. 264, 19449-19457), were tested in Jurkat tumor lymphocytes and in REF52 rat embryo fibroblasts. Both dyes could be introduced by direct microinjection. However, when cells were incubated with the tetra(acetoxymethyl) esters of the dyes, only SBFI gave intracellular loading that was reasonably responsive to [Na+]i. Because some compartmentation of the SBFI was visible and because the indicator properties are somewhat affected by cytoplasm, the relationship between intracellular free Na+ [( Na+]i and the 340/385 nm excitation ratio of the indicator was calibrated in situ using poreforming antibiotics to equilibrate cytosolic [Na+] [( Na+]i) with extracellular [Na+]. The excitation ratio was sufficiently sensitive to resolve small changes, less than or equal to 1 mM, in [Na+]i in single cells. Basal [Na+]i values in lymphocytes and serum-starved fibroblasts were 9.4 and 4.2 mM, respectively. As expected, large increases in [Na+]i were elicited by blocking the Na+ pump with ouabain or withdrawal of extracellular K+. Mitogens such as phytohemagglutinin acting on the lymphocytes, or serum or vasopressin in fibroblasts, caused [Na+]i to increase up to 2-fold. In fibroblasts, the rise in [Na+]i was due at least partly to a stimulation of Na+ influx, which was not wholly through the Na+/H+ exchanger. The mitogen-induced increases in [Na+]i and the rate of Na+ influx are consistent with earlier estimates based on measurements of total [Na+] or tracer fluxes. However, the absolute values for free [Na+]i are much lower than previous values for total intracellular Na+, suggesting that much of the latter is bound or sequestered.
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PMID:Fluorescence ratio imaging of cytosolic free Na+ in individual fibroblasts and lymphocytes. 247 59

In order to investigate the production and secretion of hypothalamic factors by the prolactin and proopiomelanocortin (POMC)-derived, peptide-producing, transplantable rat pituitary tumor 7315a, we determined the concentrations of corticotropin-releasing factor (CRF)- and vasopressin (AVP)-like immunoreactivities (IR) in the tumor extracts [14.0 +/- 1.6 (SE) and 4.2 +/- 0.9 pmol/g, respectively] and incubation media (0.26 +/- 0.01 and 0.07 +/- 0.01 pmol/10(7) cells/h, respectively). Total peptide content correlated well with tumor weight. Moreover, there is a very good correlation between the CRF and AVP IR, but not as good between CRF or AVP IR and POMC peptide IR tumor contents. Tumor extracts were chromatographed on Sephadex G-75 and compared with chromatograms of stalk median eminence (SME) extracts from normal Buffalo rats. CRF IR in tumor chromatograms gave an unusual pattern of peaks. About 31% of the total CRF IR was eluted in the high molecular weight region. The major portion of CRF IR was located in a wide region of lower molecular weight. The AVP radioimmunoassay revealed a similar pattern of peaks in tumor and SME chromatograms. A propressophysin-like peak and a smaller peak coeluting with synthetic AVP were detected. Immunohistochemical staining of consecutive sections of the tumor indicated that AVP and CRF are often found in the same cell, but the CRF and AVP-producing cells are clearly distinct from the POMC peptide-producing cells.
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PMID:Corticotropin-releasing factor and vasopressin production in the rat pituitary tumor 7315a: biochemical and immunohistochemical studies. 254 Sep 7

A case of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with Ramsay Hunt syndrome is reported. A 59-year-old man was admitted to our department for treatment of left facial pain that had persisted for three days. A left renal tumor had been diagnosed and a radical nephrectomy had been performed two months earlier. On admission, vesicular lesions were found in the left external auditory canal and ear lobe. Additionally found were left facial nerve palsy and hearing loss. Acyclovir 5 mg/kg, three times per day, was started. Five days after admission, the patient became confused and disorientated. Further investigation revealed hyponatremia 118 mEq/l, low serum osmolality, high urine osmolality, normal renal function, normal adrenal and thyroid hormones, and high plasma vasopressin 30 pg/ml. Although cerebrospinal fluid (CSF) examination revealed a mild elevation in protein and cells, no malignant cells were present and bacterial examinations were negative. Antibodies to varicella-zoster virus (VZV) in both IgG and IgM were present in high titers not only in the serum but also in the CSF. Intravenous hypertonic saline and water restriction were started, and the patient's sensorium was improved in accordance with the increase in serum sodium concentration. These results indicate that the hyponatremia in this case was due to SIADH and that SIADH was caused by an increased release of vasopressin probably because of the infection of VZV in the central nervous system.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with Ramsay Hunt syndrome: report of a case and review of the literature. 254 53

Anaplastic small cell carcinoma of the larynx is an uncommon neuroendocrine tumor. We report a case of this neoplasm of a 53-year-old male. The patient showed persistent hyponatremia accompanied with continuous loss of sodium in the urine, which resulted from inappropriate secretion of antidiuretic hormone (ADH). It is postulated that hyponatremia in this case was due to production of ADH by the tumor cells.
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PMID:Anaplastic small cell carcinoma of the larynx. 255 73

Preliminary studies are reported on the use of 131I-labelled antibodies against vasopressin associated human neurophysin to image tumors in patients with small cell carcinoma of the lung (SCCL). The rabbit polyclonal antibodies used in these studies were affinity purified on columns of neurophysin-Sepharose. Patients were pre-screened for the presence of neurophysin producing tumors by plasma RIA. Six patients who screened positive received approximately 1 mCi/70 kg body weight of radioiodinated antibody preparation, and scintigraphy was subsequently performed at 24 h, 48 h, and 72 h using a subtraction technique based on simultaneous imaging with radiopharmaceutical agents labelled with technetium-99m. Tumor was clearly demonstrated at 72 h in all five patients who had measurable lesions at the time of study, while no positive image was noted for one patient in complete clinical remission. Since approximately 70% of all SCCL patients have neurophysin-producing tumors, our findings suggest that neurophysin antibodies may be effectively used to scan tumors in a majority of patients with SCCL.
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PMID:Imaging of small cell carcinoma using 131I-labelled antibodies to vasopressin associated human neurophysin (VP-HNP) 255 81

Three clones of the pig kidney cell line LLC-PK1 were isolated and characterized with regard to morphology, growth, proximal tubule enzyme activity, sugar uptake capacity, and hormone and drug responsiveness in a defined medium. Clone N4 was similar in morphology to the wild type (WT), whereas clone F8 showed loose attachment to the substrate, formed large, sweeping domes, and had an elongated desmosome junction between cells. The third clone, F2, did not form domes and showed a marked reduction in growth rate. Cultures of WT, N4, and F8 had higher specific activities of the enzyme alkaline phosphatase and gamma-glutamyl transpeptidase at confluence relative to growing cells; however, there was no evidence of an increase in activity of either enzyme at confluence in F2. Phlorizin-sensitive alpha-methyl-D-glucoside uptake and cytochalasin B-sensitive 2-deoxy-D-glucose uptake were measured in confluent cultures grown on porous filter supports. None of the clones lacked either of the hexose transport systems, although quantitative differences were evident. N4 cells grown in a defined medium in 96-well culture plates were tested in situ for their enzyme responses to differentiation inducers, tumor promoters, and hormones. Alkaline phosphatase activity was significantly increased at confluence by serum, parathyroid hormone (PTH), and vasopressin (AVP), and was decreased by tetradecanoylphorbol acetate (TPA) and epinephrine (EPI). Glutamyl transpeptidase activity was decreased at confluence by serum, TPA, and EPI. Similar tests on alpha-methyl-D-glucoside uptake showed that serum, TPA, PTH, and AVP had no significant effect on phlorizin-sensitive uptake; however, calcitonin increased uptake by 84% (n = 18). It was concluded that LLC-PK1 clones maintained in a defined medium are useful models for studying renal cell function.
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PMID:Growth, enzyme activity, sugar transport, and hormone supplement responses in cells cloned from a pig kidney cell line LLC-PK1. 256 38

The study included 10 female donors, 12 patients with benign and 59 with malignant tumors of the breast at various stages before and after treatment. The immunomodulating effect of vasopressin and interleukin-2 on blood-natural killer functional activity was studied in vitro. Vasopressin dose of 4 x 10(-1) IU/5 x 10(5) cells exerted an immunosuppressive effect while 4 x 10(-5) IU/5 x 10(5) cells stimulated immunity. The stimulating effect of optimal interleukin-2 dosage (20-40 U/5 x 10(5) cells) on natural killer functional activity appeared 1.5-2-times higher than that optimal vasopressin dose (4 x 10(-5)/5 x 10(5) cells). Combined administration of the agents was not followed by increase in overall effect. Sensitivity of blood-natural killer cells in breast cancer patients to vasopressin and interleukin-2 depended upon clinical pattern, stage of tumor and treatment modality.
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PMID:[Immunomodulating activity of natural killers in patients with breast tumors using vasopressin and interleukin 2 in vitro]. 259 62

The pathophysiology and treatment of esophageal varices are reviewed. The cause of esophageal varices is generally thought to be portal hypertension. The most common cause of portal hypertension in the United States is alcoholic liver disease. Other etiologies of portal hypertension include portal vein thrombosis, schistosomiasis, and inferior vena caval obstruction by tumor or thrombus. Although short-term balloon tamponade and vasopressin infusion will control acute variceal hemorrhage, they do not affect the underlying problem and are not indicated for long-term treatment of esophageal varices. Surgical procedures either ablate varices or lower portal vein pressure. Portal-systemic shunts have emerged as the preferred surgical technique, but the superiority of total versus selective shunts is unclear. Pharmacological management can include administration of vasopressin, somatostatin, verapamil, or isosorbide dinitrate for short-term treatment or verapamil, isosorbide dinitrate, or propranolol for prolonged treatment. Use of sclerotherapy for treatment and prevention of hemorrhage from esophageal varices has grown recently. Because there are several sclerosing agents and combinations of agents available for use, assessing their relative safety and efficacy is difficult. Innovative approaches to management of varices include a shunt procedure involving the left lung, use of a tissue adhesive, and laser treatment. Because of its effectiveness and ease of administration, sclerotherapy appears to be a rational method of treatment for acute hemorrhage from esophageal varices.
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PMID:Treatment of esophageal varices. 264 81


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