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)

Mouse monoclonal antibody (mAb) L6 identifies an antigen expressed on the cell surface of many different human carcinomas. While studying the binding activity of mAb L6 to intracerebral tumor xenografts of human lung carcinoma LX-1 cells in nude rats using immunohistological techniques, we observed that L6 can also bind to a cytoplasmic antigen expressed in the magnocellular component of the hypothalamo-neurohypophysial system. Double-labeling experiments with antisera to vasopressin and oxytocin confirmed the localization of L6 immunoreactivity within both peptide-containing cell groups. L6 immunoreactivity in Brattleboro rats (with genetic deletion in the vasopressin gene) was exclusively localized within oxytocin neurons. Oxytocin and vasopressin failed to block L6 staining which suggested that its target epitope resides within the neurophysin sequence, and this explanation was supported by the finding that adsorption of L6 with porcine neurophysin completely eliminated hypothalamic immunoreactivity. Western blot analysis of bovine neurophysin and human pituitary extracts identified L6-immunoreactive bands which corresponded to the position of neurophysin and pro-pressophysin, confirming that L6 immunoreactivity in hypothalamus is related to neurophysin. Thus, monoclonal antibody L6, which is highly reactive with a membrane antigen of human lung cancer cell line LX-1, recognizes a cytoplasmic epitope in hypothalamic neurons identified as neurophysin by immunohistochemistry and Western analysis.
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PMID:Identification of neurophysin immunoreactivity in hypothalamus by a monoclonal antibody to a carcinoma cell surface antigen. 211 32

Hyponatremia in patients with small cell lung cancer can be caused by tumor production of arginine vasopressin (AVP) and result in the syndrome of inappropriate antidiuretic hormone. In evaluating the expression of AVP mRNA from tumor and tumor cell line specimens from five patients with small cell lung cancer and hyponatremia (presumed to have the syndrome of inappropriate antidiuretic hormone), we found that the tumors and tumor cell lines from two of these five patients expressed AVP mRNA. The RNA samples from the three patients with undetectable AVP mRNA expressed abundant atrial natriuretic factor (ANF) mRNA. Analysis of specimens from three patients with small cell lung cancer and normal serum sodium levels revealed no detectable AVP mRNA expression, and samples from only one of these three patients' specimens expressed detectable ANF mRNA. The AVP and ANF peptide levels in lysate preparations of the tumor cell lines from four of these patients were tested by radioimmunoassay and confirmed the gene expression data. These studies demonstrate ectopic production of ANF mRNA in small cell lung cancer specimens from patients with this cancer and the syndrome of inappropriate antidiuretic hormone. These findings will be of particular interest if future studies demonstrate that ectopic ANF production can cause sodium abnormalities in patients with small cell lung cancer.
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PMID:Expression of the atrial natriuretic factor gene in small cell lung cancer tumors and tumor cell lines. 215 41

The effects of cortisol, its steric analog 11-epicortisol, and lysine vasopressin (LVP) on DNA and RNA synthesis in isolated adrenocorticotropic hormone-secreting human pituitary tumor cells obtained by transsphenoidal surgery were studied using [3H]thymidine incorporation in DNA and [3H]uridine in RNA. Cortisol suppressed RNA and, to a greater extent, DNA synthesis in these cells. This could explain the slow growth of pituitary tumors in patients with Cushing's disease and the rapid growth of Nelson's pituitary tumors after bilateral adrenalectomy. 11-Epicortisol also suppressed RNA synthesis, but it had a stimulatory effect on DNA synthesis, which indicates a high specificity of glucocorticoid receptors. When applied together with cortisol, 11-epicortisol antagonized the suppressive effects of cortisol on DNA synthesis. Although LVP stimulated RNA synthesis, it suppressed DNA synthesis in most of the tumor cells.
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PMID:The effects of cortisol, 11-epicortisol, and lysine vasopressin on DNA and RNA synthesis in isolated human adrenocorticotropic hormone-secreting pituitary tumor cells. 215 95

It may sometimes be difficult to distinguish Cushing's disease from ectopic ACTH syndrome. A case is described here of a patient with a Cushing's syndrome and diagnostic difficulties. Initial features were consistent with a Cushing's disease (in particular metopirone test was positive). Because of relapse of hypercortisolism after mitotane therapy, total adrenalectomy was performed. Thereafter features occurred that evoked Nelson's syndrome, including high plasma ACTH levels and a pituitary mass syndrome. Pituitary reserve testings by vasopressin or corticotropin-releasing factor were positive, although inconstantly, in that plasma ACTH increased. A lung tumor was discovered about 20 yr after the first clinical signs of hypercortisolism. Its removal led to the discovery of a bronchial carcinoid tumor and was followed by normalization of plasma ACTH levels. An analysis of proopiomelanocortin-related peptides was performed postoperatively on the blood drawn before and after the tumor resection and on the tumor; the results of this study would have been contributive to the diagnosis of occult ectopic ACTH tumor. In conclusion this case demonstrates the limitations of the conventional procedures in the diagnosis of the ectopic ACTH syndrome. At contrast the newer biochemical procedures may be very useful in determining the type of hypercortisolism.
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PMID:A case of pseudo-Nelson's syndrome: cure of ACTH hypersecretion by removal of a bronchial carcinoid tumor responsible for Cushing's syndrome. 217 23

In this study, the author intended to examine the validity of the inhaled hydrogen gas clearance method (i-H2) for determination of the hepatic blood flow (HBF), and also to show some applicabilities of the method in experimental animals and patients with liver diseases. Simultaneous determinations of HBF by i-H2 and electromagnetic flowmetry in rabbits revealed an excellent correlation between the values obtained by the two methods. Moreover, HBF in rabbits measured by i-H2 varied in parallel with that by thermocouple flowmetry or laser Doppler velocimetry after administration of norepinephrine, propranolol or glucagon. In carbon tetrachloride-treated rats, HBF measured by i-H2 correlated better with the severity of damage in the sinusoidal structure than the severity of hepatic cell injury or the serum levels of transaminases. HBF as determined by i-H2 was significantly decreased in acute hepatitis (AH), chronic inactive hepatitis (CIH), chronic active hepatitis (CAH), liver cirrhosis (LC) and fatty liver. Reduced HBF in AH returned to normal during recovery of the disease. The ratio of HBF in tumor/normal tissue was greater than 1.0 for hepatocellular carcinoma in contrast to the ratio of less than 1.0 for metastatic liver carcinoma. Propranolol caused a decrease in HBF by 31%, and vasopressin by 39% in patients with CIH or LC. In contrast, glucagon induced its increase by 65%, 35% and 17%, respectively, in patients with CIH, AH and LC.
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PMID:[Measurement of hepatic blood flow by the hydrogen gas clearance method. Experimental and clinical observations]. 236 96

Bombesin (BN), a tetradecapeptide neuropeptide growth factor, is shown to be a potent (ED50 of 5 X 10(-12) M) chemoattractant for human monocytes and small cell lung carcinoma cells (SCCL). These effects are BN receptor-mediated since potencies of several BN analogs to induce chemotaxis and to inhibit [125I-tyr4] BN binding activity correlate well (P less than 0.001). As has been demonstrated for other BN receptor-mediated effects, carboxy-terminal amino acids are required for optimum biological activity. BN is not an exclusive chemoattractant for SCCL cells but was also active in promoting migration of other, but not all, lung tumor cells. Other neuropeptides, such as beta-endorphin, substance P, and arg-vasopressin, are also shown to be chemoattractants for SCCL cells, with EC50's also in the 10(-12) M range. The ability of these ligands to effect monocyte and some tumor cell migration suggest a role for neuropeptides in inflammation and metastasis. In the latter case, tumor cells, in response to neuropeptide chemical gradients, may become localized at specific body sites. Neuropeptide release, in response to cognitive or other stimuli, may thereby modify cell migratory patterns. Additionally, such hormones may influence early developmental events such as tissue organization and histogenesis.
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PMID:Neuropeptides are chemoattractants for human tumor cells and monocytes: a possible mechanism for metastasis. 241 46

Cholecystokinin octapeptide (CCK-8) stimulated adrenocorticotropin hormone (ACTH) release from both rat anterior pituitary cells in culture and a tumor cell line of the mouse anterior pituitary (AtT-20/D16-16). The stimulation of ACTH release was dependent on the time of exposure to CCK-8 and the concentration of this peptide applied to anterior pituitary cells. Cerulein evoked ACTH release whereas human gastrin 1, CCK-4 and desulfated CCK-8 only produced minimal affects on ACTH release at concentrations of 10(-4) M. In contrast, these latter three peptides were as effective as CCK-8 in inducing the secretion of amylase from pancreatic acinar cells. Antagonists of CCK-8 receptors in the pancreas such as proglumide, benzotript and dibutyryl cyclic GMP did not affect the ACTH release response to CCK-8. The CCK-8 stimulation of ACTH release was calcium-dependent and blocked by glucocorticoid pretreatment. The mechanisms by which CCK-8 evoked ACTH release appears distinct from that of other ACTH secretagogues such as corticotropin releasing factor and vasopressin. The data suggest that CCK-8 is a corticotropin releasing factor-like agent acting through a putative novel receptor subtype in the anterior pituitary.
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PMID:Cholecystokinin-8 stimulates adrenocorticotropin release from anterior pituitary cells. 241 42

Small cell carcinomas of the prostate gland are rare, and their histogenesis and clinical behavior remain poorly defined. We report a case with antidiuretic hormone secretion, which demonstrates direct transformation of the adenocarcinoma into the small cell component. The adenocarcinoma reacted positively for prostatic antigen, and negatively for carcinoembryonic antigen and neuron specific enolase, whereas the small cell component was negative for prostatic antigen, and positive for carcinoembryonic antigen and neuron specific enolase. At biopsy this was interpreted as denoting 2 separate tumors: one of prostatic and the other of nonprostatic origin. The clinical course was rapidly fatal but otherwise manifested the metastatic pattern of prostatic carcinoma. We caution that immunohistochemical reactions may be misleading if not interpreted in the context of other findings in the case. This case is labeled as a small cell carcinoma rather than a poorly differentiated adenocarcinoma of the ordinary type because the tumor exhibited morphological, immunohistochemical and biological features typical for that neoplasm.
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PMID:Small cell carcinoma of the prostate gland with inappropriate antidiuretic hormone secretion: morphological, immunohistochemical and clinical expressions. 242 10

Receptors for the hormones vasopressin, angiotensin II, and thyrotropin-releasing hormone have been studied electrophysiologically in Xenopus laevis oocytes previously injected with poly(A)+ RNA from the respective receptor-containing tissues. The injected oocytes responded to the hormones by demonstrating oscillations in membrane currents as recorded by the voltage-clamp method. The response was dependent on the hormone concentrations and detectable between 5 and 1000 nM concentrations. Size fractionation of poly(A)+ RNA from the respective tissues showed that the mRNAs encoding the three hormone receptors were larger than 18S rRNA, suggesting a length of at least 2 kilobases. When vasopressin was added to the oocyte bath, an inward membrane current was generated in oocytes injected with rat poly(A)+ RNA from liver but not from kidney. This suggests that the V1-type (liver), not the V2-type (kidney), vasopressin receptor can be expressed and electrophysiologically identified in the oocyte. A V1-specific, but not a V2-specific, antagonist suppressed the vasopressin-dependent effect. Application of angiotensin II to liver poly(A)+ RNA-injected oocytes elicited oscillations in membrane current, indicating that these oocytes also expressed receptors for angiotension II; the antagonist [Sar1, O-methionyl-Tyr4]angiotensin II blocked this effect. Poly(A)+ RNA from tumor-derived GH3B6 cells, known to contain receptors for thyrotropin-releasing hormone, injected into oocytes induced receptors responding to thyrotropin-releasing hormone; the drug chlordiazepoxide suppressed the thyrotropin-releasing hormone response.
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PMID:Receptors for neuropeptides are induced by exogenous poly(A)+ RNA in oocytes from Xenopus laevis. 244 81

Stimulation of phosphatidylinositol metabolism by neurotransmitters produces diacylglycerol, an activator of protein kinase C, which may be involved in hormone-mediated contractions. We studied the effect of a tumor-promoting phorbol ester, 12-deoxyphorbol 13-isobutyrate 20-acetate (DPBA), on contraction of caudal artery rings of Wistar-Kyoto control (WKY) and spontaneously hypertensive rats (SHR) in order to examine whether protein kinase C-mediated mechanisms are increased in SHR. Although DPBA alone did not produce contractions of either WKY or SHR caudal artery rings, it greatly potentiated the contractions evoked by norepinephrine, norepinephrine, vasopressin, potassium, and calcium ionophore A23187. The potentiation of contractile response to these agents by DPBA was dependent on extracellular calcium. The DPBA potentiation of contractions evoked by norepinephrine, vasopressin, and potassium was significantly greater (p less than 0.05) in SHR than in WKY, while no differences were observed between strains for the contractions evoked by calcium ionophore A23187. These results indicate that the protein kinase C-mediated responses are increased in SHR caudal artery rings, and this effect appears to be due to increased calcium influx through cell membrane calcium channels.
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PMID:Contractile response of spontaneously hypertensive rat caudal artery to phorbol esters. 245 63


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