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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possibility of covalently attaching vasopressin to its receptors by the use of a bifunctional reagent was explored. Plasma membranes from the LLC-PK1 pig kidney cell line were purified by Percoll density gradient centrifugation. These membranes contained a single population of high affinity (Kd = 5.2 nM) and high capacity (Bmax 3.8 pmol/mg of protein) [3H]lysine vasopressin ([3H]LVP)-binding sites. [3H]LVP-labeled receptors could be solubilized with a high yield (83%) and minimal dissociation (9%) by treatment with the non-ionic detergent, octaethylene glycol mono-n-dodecyl ether (C12E8) (0.5%, v/v) in the presence of glycerol (20%). The solubilized [3H]LVP-labeled receptors were stable upon storage at 4 degrees (5% dissociation after 24 hr). They were partially purified to a specific activity of 17 pmol/mg of protein by chromatography on a Cibacron blue-Sepharose column with a yield of 90%. The [3H]LVP-receptor complexes in both intact membranes and the partially purified preparation were almost completely dissociated by incubation at 30 degrees for 30 min in the presence of 20 mM ethylenediaminetetraacetate (EDTA). This property was used to test the effect of ethylene glycol bis (succinimidyl-succinate) (EGS) as cross-linking reagent for the covalent attachment of [3H]LVP to its receptors. After treatment of [3H]LVP-labeled membranes for 30 min with 1 mM EGS at 4 degrees, about 30% of specifically bound [3H]LVP was resistant to EDTA dissociation. The amount of EDTA-resistant binding varied as a linear function of the fractional receptor occupancy and maximal binding capacity of the different batches of membranes used. Similar results were obtained with solubilized and partially purified vasopressin receptors. Upon steric exclusion high performance liquid chromatography, the EDTA-resistant [3H]LVP-labeled material, like the native [3H]LVP-labeled receptor, was eluted as a single and apparently homogeneous peak. The covalent character of the EGS-induced [3H]LVP binding to solubilized or partially purified receptors was assessed by its resistance to sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). The yield of EGS-induced labeling deduced from these experiments (27%) was close to that determined by the EDTA method. SDS-PAGE analysis of the [3H]LVP-labeled cross-linked material revealed the specific labeling of a major 50-kDa component and a minor component of 30 kDa. The size of these two components was not affected by dithiothreitol.
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PMID:Covalent labeling of vasopressin receptors from LLC-PK1 cells by the use of a bifunctional reagent. 296 89

We have improved a radioimmunoassay for arginine-vasopressin (AVP) and atrial natriuretic peptide (ANP) by using Sep-Pak C18 cartridges to extract AVP and ANP from acidified plasma. The analytes are co-eluted by use of a mobile phase consisting of 1,2-dimethoxyethane and 40 g/L aqueous trifluoroacetic acid (95/5, by vol). After rapid evaporation of the solvents, AVP and ANP are assayed by a nonequilibrium radioimmunoassay method in which commercially available antibodies and radiolabeled antigens are used. The bound fractions are separated from the free by use of polyethylene glycol with human gamma globulin and rabbit anti-human IgG as the second antibody. This results in very low nonspecific binding: 0.44% for the ANP assay, 0.70% for AVP. The minimum detectable amount of ANP is 0.39 pg per tube; for AVP, it is 0.13 pg per tube. Compared with other published methods, this method is substantially more reliable, economical, and easily established in a clinical chemistry laboratory.
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PMID:Rapid, simplified radioimmunoassay of arginine-vasopressin and atrial natriuretic peptide in plasma. 296 31

Atractyloside inhibited gluconeogenesis from dihydroxyacetone in hepatocytes from fasted rats and increased lactate synthesis. In the presence of atractyloside, lactate/pyruvate and beta-hydroxybutyrate/aceto-acetate ratios were increased and the accumulation of Fru-2,6-P2 was prevented. In the absence of atractyloside, gluconeogenesis from dihydroxyacetone was stimulated by dibutyryl-cAMP and, to a much lesser extent, by norepinephrine and vasopressin. Omission of Ca2+ increased the stimulation by norepinephrine but prevented that by vasopressin. High concentrations (greater than or equal to 40 microM) of atractyloside abolished the stimulation of gluconeogenesis by dibutyryl-cAMP but not that by norepinephrine or vasopressin. Exogenous Ca2+ was not required for hormonal stimulation in the presence of atractyloside. The stimulation by norepinephrine was inhibited by ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N-tetraacetic acid or prazosin but not by propranolol. Atractyloside caused decreases of all glycolytic intermediates and an activation of pyruvate kinase. Norepinephrine partially reversed these effects. The mitochondrial and cytosolic ATP/ADP ratios were determined by digitonin fractionation of hepatocytes. Norepinephrine or vasopressin increased the cytosolic ATP/ADP in the presence of atractyloside. We suggest that the increased availability of cytosolic ATP could be responsible for the stimulation of gluconeogenesis by these hormones.
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PMID:Catecholamine and vasopressin stimulation of gluconeogenesis from dihydroxyacetone in the presence of atractyloside. 299 83

Calcium-sensitive inositide release in a purified rat liver plasma membrane preparation is increased by calcium-mobilizing hormones in the presence of guanine nucleotides. Vasopressin-stimulated inositide release is evident in the presence of GTP or its nonhydrolyzable analogs guanyl-5'-yl imidodiphosphate and guanosine 5'-(3-O-thio)triphosphate (GTP gamma S). The stimulation of inositide release by (-)-epinephrine (alpha 1), angiotensin II, or vasopressin in the presence of either 1 microM or 10 microM GTP gamma S correlates with the number of receptors present for each hormone. The guanine nucleotide and hormonal stimulation is evident on both inositol trisphosphate production and phosphatidylinositol bisphosphate degradation. Ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (1 mM) completely abolishes stimulation by guanine nucleotides and hormone. Prior treatment of plasma membranes with cholera toxin or islet activating protein or prior injection of animals with islet activating protein does not affect stimulation of inositide release by GTP gamma S or GTP gamma S plus vasopressin. Stimulation by GTP gamma S is dependent upon magnesium and is inhibitable by guanosine 5'-(2-O-thio) diphosphate. Inositide release from the plasma membrane exhibits half-maximal stimulation by calcium at approximately 100 nM free calcium in the presence of 1.5 mM MgCl2 and at approximately 10 microM free calcium in the presence of 10 mM MgCl2. Addition of guanine nucleotides decreases the requirement for calcium and also increases the activity at saturating calcium. The results presented suggest that calcium-mobilizing hormones stimulate polyphosphoinositide breakdown in rat liver plasma membranes through a novel guanine nucleotide binding protein.
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PMID:Hormone-stimulated polyphosphoinositide breakdown in rat liver plasma membranes. Roles of guanine nucleotides and calcium. 300 97

The role of the renin-angiotensin system as a mediator of water intake, induced by hypovolemia after polyethylene glycol (PEG) injection, was investigated. Blockade of angiotensin I converting enzyme and of angiotensin receptors was used as a pharmacological tool. A significant reduction of water intake was observed when angiotensin I converting enzyme was inhibited by captopril and enalapril. In PEG-treated rats with blockade of angiotensin I converting enzyme, hypertonic saline injection continued to elicit substantial drinking. Normalization of low blood pressure by vasopressin infusions in PEG and captopril treated rats did not interfere with the antidipsogenic effectiveness of converting enzyme blockade. The angiotensin II receptor antagonist, saralasin, also reduced PEG-induced drinking although less effectively than converting enzyme inhibitors. We conclude that water intake due to isotonic depletion of the extracellular fluid compartment may depend on the activity of the renin-angiotensin system.
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PMID:Renin-dependent water intake in hypovolemia. 306 73

Abnormalities in the vasopressin (VP) and renin-angiotensin systems have been described in spontaneously hypertensive rats (SHR). Responsiveness of these systems to a decrease in plasma volume was examined in the SHR at 6, 8, and 18 wk of age and compared with responses in age-matched normotensive Wistar and Wistar Kyoto rats (WKY). Trunk blood was collected 3 h after administration of 2 ml/100 g body wt of 0.9% saline, 15 or 30% polyethylene glycol (PEG), and in one group of conscious 8- and 18-wk-old rats, mean arterial pressure was monitored following PEG administration. Hematocrit and serum VP increased significantly in both strains at all ages following PEG. At 6 and 8 wk of age, the VP response to the PEG injection was significantly greater in SHR compared with WKY (P less than 0.005), but at 18 wk the response was comparable in the two strains. Serum renin activity (SRA) also increased in both strains receiving PEG at 6 and 8 wk of age, but the response was suppressed in the SHR relative to the WKY (P less than 0.001). At 18 wk of age, SRA increased in WKY, but the response was totally suppressed in SHR. Renal renin content in a separate group of rats was reduced in 19-wk-old SHR compared with WKY (P less than 0.001) but was not different in 5- and 8-wk-old rats. Thus there appears to be a hyperresponsiveness in the VP system in young SHRs that is not present in the renin-angiotensin system. The divergence in the responsiveness of the renin and VP systems and the attenuation of responsiveness in the VP system in 18-wk SHRs indicate a differential effect of the hypertensive process on the VP and renin systems in the SHR.
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PMID:Vasopressin and renin response to plasma volume loss in spontaneously hypertensive rats. 351 27

Isosmotic volume depletion was induced by subcutaneous injection of 5 ml of polyethylene glycol (PEG; 20 M; 30%) in Long-Evans rats and in rats deficient in hypothalamic vasopressin (Brattleboro rats). In the PEG-treated Long-Evans rats, captopril caused a hypotension that was greater than that seen in saline-injected controls. Pretreatment with the vasopressin (V1 receptor) antagonist d(CH2)5DAVP did not, itself, cause a fall in blood pressure, but it enhanced the hypotensive effect of captopril in the PEG-treated Long-Evans rats. The PEG-treated Brattleboro rats had similar resting blood pressures to the PEG-treated Long-Evans rats, but in the former group, captopril caused a more profound and progressive hypotension than was seen in any of the present experimental regimes used in the Long-Evans rats. This suggests that, during hypovolemia induced by PEG, Brattleboro rats were either more dependent on the renin-angiotensin system for the maintenance of arterial blood pressure than were Long-Evans rats treated acutely with a vasopressin (V1) receptor antagonist or less able to recruit sympathoadrenal mechanisms to compensate for the sudden loss of the renin-angiotensin system.
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PMID:Pressor contributions from angiotensin and vasopressin after polyethylene glycol. 353 27

Fluid balance, systolic blood pressure (BP) and serum vasopressin (VP) and renin activity (SRA) in the basal state and in response to blood volume depletion were examined in unanesthetized rats previously given intrathecal 6-hydroxydopamine (6-OHDA) to destroy catecholaminergic (CA) input to supraoptic nucleus (SON). Sham-operated rats, unoperated ad libitum hydrated rats and rats undergoing 4 days of water deprivation served as controls. The 6-OHDA lesion resulted in adipsia, a failure to conserve administered fluids and a decrease in systolic BP. Despite decreased blood volume secondary to dehydration, and decreased systolic BP, the 6-OHDA group failed to show the expected increase in serum VP. However, when blood volume was further decreased following intraperitoneal polyethylene glycol, lesioned rats showed robust VP and SRA responses. Thus, CA input to critical target areas in the hypothalamus may be necessary for maintenance of sensitivity to stimuli that normally elicit VP release. Decreased systolic BP following 6-OHDA lesions most likely results from dehydration coupled with inadequate VP responses.
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PMID:Effects of lesions of hypothalamic catecholamines on blood pressure, fluid balance, vasopressin and renin in the rat. 355 13

Subcutaneous injection of polyethylene glycol (PEG) solution in rats produces exponential increases in secretion of arginine vasopressin (AVP) and oxytocin (OT) in proportion to the induced plasma volume deficits. Previously, we reported that acute water loads eliminated the neurohypophyseal hormone responses to hypovolemia, whereas hypertonic NaCl potentiated them. The present experiments indicated that AVP and OT secretion after PEG treatment were blunted by prior maintenance of rats on a sodium-deficient diet for 2 days. In contrast, plasma AVP and OT levels after PEG treatment were enhanced by prior adrenalectomy or ligation of the inferior vena cava or by concurrent administration of phentolamine in association with arterial hypotension. AVP and OT responses to hypovolemia were similarly potentiated in rats made uremic by bilateral nephrectomy or by puncturing their bladders. These results parallel previous findings that osmotic dilution and sodium deprivation each enhance the sodium appetite induced by PEG treatment in rats, whereas hyperosmolality, hypotension, and uremia each abolish it. Consequently, they support our previous hypothesis that sodium appetite is inversely related to the activity of hypothalamic oxytocinergic neurons.
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PMID:Neurohypophyseal secretion in hypovolemic rats: inverse relation to sodium appetite. 357 55

The effects of i.p. injected hypertonic NaCl and polyethylene glycol on the magnitude of increase in plasma vasopressin after footshocks were studied in male rats, to determine whether hypovolemia and body fluid osmolality interact with noxious stimuli on vasopressin secretion. Present data have demonstrated that non-osmotic hypovolemia but not body fluid hyperosmolarity interact significantly and synergistically with footshocks to potentiate vasopressin secretion.
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PMID:Synergistic interactions between footshocks and non-osmotic hypovolemia on vasopressin secretion in rats. 358 Aug 93


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