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 distribution of gonadotropin-releasing hormone (GnRH) was studied in the brain and infundibulum (INF) or median eminence of sheep utilizing a peroxidase-antiperoxidase immunohistochemical method. This procedure utilized a specific antiserum generated against GnRH conjugated to bovine serum albumin. In the rostral INF, the greatest concentration of GnRH positive axons was found in the medial region, mostly in the external layer dorsal to the hypophysial portal plexus. In the intermediate portion of the INF, the hormone was mainly observed in the external layer at the more dorsolateral areas ventral to the tuberoinfundibular sulcus. GnRH was generally located medially in the caudal portion of the INF and dorsomedially in the rostral infundibular stalk. Substantial amounts of reaction product were also noted in the internal layer throughout the entire rostrocaudal extent of the INF. The hormone was localized in axons throughout the brain from the septal and medial preoptic areas to the mammillary bodies. GnRH-positive perikarya were scattered in various regions of the infundibular (arcuate) and for the first time in the ventromedial nuclei of sheep hypothalamus. Preabsorption of the specific antiserum with synthetic GnRH abolished staining in both axons and perikarya, whereas preabsorption with thyrotropin-releasing hormone, oxytocin, arginine-vasopressin, and adrenocorticotrophic hormone did not affect staining intensity.
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PMID:Immunohistochemical localization of gonadotropin-releasing hormone (GnRH) in the brain and infundibulum of the sheep. 701 81

The biosynthesis of [arginine8]vasopressin (AVP) and oxytocin (OT) was studied, and the results obtained have been compared with a study of their associated neurophysins (NP), AVP-NP and OT-NP. Rat hypothalamic extracts obtained at acid pH were subjected to Sephadex G-75 gel filtration chromatography and sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis (PAGE). Fractions of gel chromatography effluent and extract of SDS-PAGE gel slices were subjected to RIA for immunoreactive precursors of AVP, AVP-NP, OT, and OT-NP using specific antisera fro each molecule. Tritiated bovine serum albumin, ovalbumin, and cytochrome c were used as internal standards during gel filtration chromatography and SDS-PAGE. Molecular weight estimates obtained for precursors of AVP were more than 70K, 31K, 13K, 5K, and less than 5K (AVP) by G-75 chromatography and more than 70K, 39K, 15K, and less than 5K (AVP) by SDS-PAGE. Molecular weight estimates obtained for precursors of AVP-NP were more than 70K, 35K, 24K, and 12K (AVP-NP) by G-75 chromatography and 19K and 10K (AVP-NP) by SDS-PAGE. Molecular weight estimates of OT were more than 70K, 35K, 19K, 8K, and less than 5K (OT) by G-75 chromatography and 60K, 35K, 19K, 9K, and less than 5K (OT) by SDS-PAGE. Precursors of OT-NP were estimated to be more than 70K, 17-18K, and 10K (OT-NP) by G-75 chromatography and 28K, 18K and 10K (Ot-NP) by SDS-PAGE. These studies show that there are small differences in precursor processing among AVP, AVP-NP, and OT, OT-NP, but allow for the existence of common precursors for AVP and AVP-NP and for OT and OT-NP.
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PMID:Putative precursors of vasopressin, oxytocin, and neurophysins in the rat hypothalamus. 728 61

Proteins of the hypothalamo-neurohypophysial system of the rat were studied by means of a purpose-modified form of microelectrophoresis in the polyacrylamide gradient. The respective shares of neurophysins I, II and III in total neurophysin were found to be 58 +/- 16, 24 +/- 5 and 18 +/- 6% in HCl extracts and 48 +/- 7, 30 +/- 7 and 23 +/- 5% in aqueous extracts. In particular, neurophysin I was absent in homozygous Brattleboro rats, with no evidence being obtained as to aberrant neurophysins. Approximately equal neurophysin shares were observed for heterozygous Brattleboro rats. Using perfused material, one of the fractions occurring in neurohypophysial extracts was clearly identified as serum albumin. The electropherograms of aqueous neurohypophysial extracts revealed up to 43 protein fractions. Comparison with extracts from the median eminence, the nuclei of the hypothalamo-neurohyophysial system and other hypothalamic regions, as well as the results of incubation experiments distinguished one fraction as a possible candidate for the hitherto hypothetical neurophysin precursors. Incubation of neurohypophyses did not yield any signs of both conversion of neurophysin II into neurophysin III, and formation of further neurophysin derivatives.
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PMID:Identification and metabolic differentiation of rat neurophysins: a microelectrophoretic study. 737 4

Nephrotic syndrome is characterized by water and sodium retention, which leads to edema formation. The nonosmotic stimulation of arginine vasopressin (AVP) release from the pituitary gland has been implicated to be one of the important factors of abnormal water retention in patients with nephrotic syndrome. It is not known, however, whether nephrotic syndrome is associated with stimulation of hypothalamic vasopressin gene expression. Puromycin aminonucleoside is known to cause altered glomerular permeability, which results in experimental nephrotic syndrome in rats. In the present study, therefore, AVP gene expression has been studied in the hypothalamus of rats with puromycin aminonucleoside-induced nephrotic syndrome (PNS). Nephrotic syndrome was induced by a single intravenous injection of puromycin aminonucleoside (50 mg/kg body weight). Nephrotic syndrome was confirmed by urinary protein excretion (control 20.8 +/- 3.5 mg/24 hr v PNS 273.9 +/- 41.4 mg/24 hr; P < 0.0001, n = 6) and serum albumin concentrations (control 4.52 +/- 0.07 g/dL v PNS 2.96 +/- 0.22 g/dL; P < 0.001, n = 6). In PNS rats, plasma AVP was significantly higher than in control rats (control 0.77 +/- 0.10 pg/mL v PNS 2.13 +/- 0.42 pg/mL; P < 0.005, n = 12), even though there were no differences in plasma osmolality (control 292.0 +/- 2.0 mOsm/kg H2O v PNS 290.3 +/- 2.5 mOsm/kg H2O; P = NS, n = 12) or serum sodium concentration (control 142.7 +/- 0.7 v PNS 142.1 +/- 1.1; PNS, n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Arginine vasopressin gene expression in rats with puromycin-induced nephrotic syndrome. 781 May 34

Serum albumin is the most abundant protein synthesized by liver cells, and its production is a reliable indicator of the differentiated state of hepatocytes. We have recently shown that fetal rat hepatocytes cultured under proliferative conditions, i.e., in the presence of EGF, responded to glucagon and noradrenaline increasing albumin protein and mRNA levels (de Juan et al., 1992. J. Cell. Physiol., 152:95-101). This effect was mimicked by agents that increase cyclic AMP levels. In this report, we show that in regenerating liver, noradrenaline modulation of albumin expression seems to be different. Hepatocytes from hepatectomized rats were cultured at low cell density and in the presence of EGF. Under these conditions, noradrenaline, which acted synergistically with EGF increasing DNA synthesis (de Juan et al., 1992. Exp. Cell. Res., 202:495-500), produced a decrease in albumin mRNA levels. This effect was dose-dependent, being maximum at 1 microM noradrenaline. Noradrenergic effect seemed to be mediated by alpha 1-receptors, because it was blocked by prazosin, but not by propranolol. Other Ca(2+)-increasing agents, as vasopressin, angiotensin II, or ATP, did not produce any effect. However, albumin mRNA levels decreased when the cells were incubated in the presence of tetradecanoyl phorbol-13-acetate (TPA). In addition, noradrenergic modulation of albumin expression was blocked by staurosporine, a protein kinase inhibitor with relative specificity for protein kinase C. Thus we can conclude that the role of noradrenaline on the regulation of liver growth and differentiation changes from fetal to adult life. This change is probably due to its action on different receptors: beta-receptors in fetal hepatocytes and alpha 1-receptors in the adult liver.
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PMID:Noradrenergic modulation of albumin expression in growth-stimulated adult rat hepatocytes in primary culture. 812 74

Adult rat primary hepatocytes maintained in DMEM/F12 (Ham) media were used as a model system for studying the role of fetal calf serum (FCS) and agonists of the phosphoinositide cascade in the metabolism of metallothionein (MT) and alkaline phosphatase (ALP). Experiments were performed both after a 24 h preincubation with FCS and with bovine serum albumin (BSA). Hepatocytes were treated with dexamethasone (DEX), zinc (Zn) and with the agonists of the phosphoinositide cascade A23187, 1,2-dioctanoyl-sn-glycerol (DiC8), 12-O-tetradecanoylphorbol-13-acetate (TPA), angiotensin II (AT), platelet activating factor (PAF), Arg8-vasopressin (VP) and were analyzed for MT and ALP activity in cell homogenates. Cell viability was evaluated by lactate dehydrogenase (LDH) liberation into culture medium, induction of tyrosine aminotransferase (TAT) through DEX and by trypan blue exclusion. Overall, cell viability was improved by the FCS pretreatment and by DEX. Exposure of hepatocytes to the established direct inducers Zn and DEX of MT resulted in a manifold increase in MT, independent of whether the cultures were FCS pretreated or not. The FCS preincubation produced a moderate elevation of ALP activity by stimulating cell viability. However, ALP was unaltered in response to Zn and DEX. None of the experiments conducted with agonists of the phosphoinositide cascade led to an elevation of MT and ALP. Only the incubation of hepatocytes with A23187 resulted in a concentration dependent significant decrease of MT and ALP. This observation was due to a cytotoxic effect of A 23187, displayed by LDH leakage and an increase in the number of cells stained with trypan blue. In conclusion, in primary hepatocyte cultures agonists of the phosphoinositide did not have an effect on the metabolism of MT and ALP. Previous in vivo results indicating alterations of Zn metabolism in liver, therefore seem to be caused by indirect systemic responses.
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PMID:Studies on the metabolism of metallothionein and alkaline phosphatase of adult rat primary hepatocyte cultures: role of fetal calf serum and agonists of the phosphoinositide cascade. 823 77

In common with many other animal cells in culture, BHK21, CHO and NIH-3T3 cells adopt bizarre stellate or arborized shapes when exposed, in the absence of serum, to agents which increase cytoplasmic cyclic AMP (cAMP). Dibutyryl cAMP, 3-isobutyl-1-methylxanthine, 5'-deoxy-5'-methylthioadenosine, cholera toxin and the invasive adenylate cyclase from Bordetella pertussis all induce similar shapes. Time lapse video recording of BHK21 cells spreading on fibronectin shows that stellate shapes are generated by outgrowth of neurite-like processes led by small fans of ruffling membrane. These structures stain strongly for F actin, and their outgrowth is completely inhibited by cytochalasin D. Thus if stellation is caused by microfilament depletion, this must be selective for subsets of microfilaments. We have quantified the shape changes of BHK21 cells using the parameter dispersion. They are prevented by low concentrations (1% by volume and below) of bovine sera. The inhibitory component of foetal bovine serum acts humorally, behaves as a macromolecule and is itself inhibited by suramin, but platelet-derived growth factor, insulin, vasopressin and bradykinin are inactive. The inhibitory activity of serum may be due to phospholipids, since it can be replaced by lysophosphatidic acid in the presence of serum albumin.
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PMID:Shapes of cells spreading on fibronectin: measurement of the stellation of BHK21 cells induced by raising cyclic AMP, and of its reversal by serum and lysophosphatidic acid. 838 76

A new method for concentrated ascitic fluid reinfusion using a double ultrafiltration device is reported as 22 procedures in 20 cirrhotic patients (6 females, 14 males; median age 55 years, range 33-69) with tense, refractory ascites. Eight of the 20 patients had elevated creatinine levels. The mean time for each procedure was 189 +/- 82 min, during which a mean of 7.7 liters (1.3-13.3) of ultrafiltered ascitic fluid was removed and 613 ml (140-1700) of concentrated ascitic fluid rich in albumin (mean: 60 g, range 14-175) was reinfused. The procedure resulted in a mean weight loss of 8.1 kg (2.2-14.0) and a mean increase of 163 ml in urine output (24 hr). A reduction in the serum creatinine level (P < 0.05) and an increase in the plasma atrial natriuretic factor level (P < 0.02) 24 hr after reinfusion, while no changes in serum albumin, plasma and urinary electrolytes, plasma renin activity, aldosterone, and antidiuretic hormone levels were noted. Although minor evidence for a disturbance in coagulation was observed, there were no episodes of clinical bleeding. Four patients (20%) had transient chills or fever. Based upon this experience, it can be concluded that reinfusion of cascade filtered and concentrated ascitic fluid is a rapid, safe, and effective treatment for patients with tense ascites; it appears to have less side effects than more traditional methods and importantly does not require administration of heterologous plasma derivatives.
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PMID:Concentrated ascitic fluid reinfusion after cascade filtration in tense ascites. 848 89

Medical treatment of cirrhotic ascites is essentially supportive, dictated by the patient's discomfort, impaired cardiovascular or respiratory function and potential for infection. Treatment of 'simple' ascites (moderate fluid accumulation, serum albumin > 3.5 g/dl, serum creatinine < 1.5 mg/dl, no electrolyte disturbance) is implemented sequentially. Only 10% of patients respond to dietary sodium restriction and bed rest; most require pharmacotherapy consisting of spironolactone, which increases the proportion of responding patients to 65% and loop diuretics, which may produce clinical improvement in an additional 20% (85% in all); in the remaining 15% of refractory patients, use of novel adjunctive therapies may be attempted. Patients with tense ascites, impaired renal function and electrolyte disturbances merit special consideration before diuretics are introduced. Spironolactone has long been a standard for the treatment of cirrhotic ascites because it directly antagonizes aldosterone. The loop diuretic most frequently added to spironolactone has been furosemide. However, there is preliminary evidence that torasemide may be more effective in some patients. Other investigational agents that may play a role in treatment of patients resistant to conventional drugs include ornipressin (a vasopressin analogue) and atrial natriuretic factor.
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PMID:Medical treatment of ascites in cirrhosis. 849 70

Previous studies by the authors demonstrated that the response of urinary aquaporin-2 (AQP2) excretion to dDAVP (deamino-8-D-arginine vasopressin) infusion is an index of vasopressin action on the kidney (N Engl J Med 332: 1540-1545, 1995). In the study presented here, the characteristics of urinary excretion of AQP2 were examined further. An RIA suitable for AQP2 in the urine was established. Relatively high concentrations of detergent and bovine serum albumin in the RIA buffer allowed analysis of urine samples with a wide range of concentrations and increased the sensitivity of the assay. AQP2 in the urine existed as a high molecular weight form of approximately 190 kD by HPLC analysis. The mean urinary AQP2 concentration corrected for creatinine in spot urine samples of healthy subjects who voided in the morning was 1081 +/- 699 fmol/mg creatinine (mean +/- SD, n = 208). The amount of daily excretion of AQP2 in the urine was the same in men and women. Urinary AQP2 content was not affected by age of the subjects and showed a positive correlation with urine osmolality. Finally, the fraction of AQP2 excreted in the urine compared with whole kidney content was determined in the rat. Approximately 3% of AQP2 in the kidney was excreted daily, and this fraction did not change when rats were dehydrated for 3 d. These data demonstrate the necessity of establishing well-designed protocols to use urinary AQP2 as a marker of AVP action.
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PMID:Urinary excretion of aquaporin-2 water channel protein in human and rat. 929 26


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