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)

Previous studies have indicated the existence of natriuretic factors of hormonal nature with the posterior pituitary gland as a possible site of origin. It was in this light that a series of experiments was designed to examine the posterior pituitary for such factors. Acetic acid extracts of porcine and bovine posterior pituitary lobe tissue were subjected to gel filtration on Sephadex G-25. Several fractions in the molecular size range of 1000 were obtained which possessed potent natriuretic activity as assayed in rats. The activity of these fractions maximally increased sodium excretion to 6-8 muequiv./min, a 10- to 40-fold increase above control, when administered intraperitoneally to hydropenic, conscious rats. However, oxytocin and vasopressin, present in the posterior pituitary are natriuretic. These hormones were measured by radioimmunoassay, and invariably only those fractions which contained vasopressin and (or) oxytocin possessed natriuretic activity. Moreover, the extent of the natriuresis could be accounted for by the vasopressin and (or) oxytocin content of the test fractions. The natriuretic property of this material was abolished by treatment with thioglycollate. Further purification of natriuretic fractions by ion exchange resins, thin-layer chromatography and isoelectric focusing failed to resolve natriuretic activity from vasopressin and oxytocin. Similar results were observed following analysis of fractions isolated by gel filtration of acetic acid extracts of ventral hypothalamus tissue. The natriuretic fractions isolated from hypothalamic tissue were indistinguishable from oxytocin and vasopressin. These experiments suggest that the natriuretic activity in neurohypophyseal extracts can be attributed to oxytocin and vasopressin.
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PMID:Characterization of natriuretic activity from posterior pituitary lobes. 97 83

Peritoneal cells from thioglycollate-stimulated mice were allowed to adhere to coverglasses for 2 h to give a dense monolayer of adherent cells greater than 95% of which were macrophages. After incubation with the tetra-acetoxymethyl ester of quin2, coverglasses were rinsed with Ca2+-free saline, oriented at a 45 degree angle in square cuvettes containing a magnetically driven stir bar, and analyzed for changes in quin2 fluorescence in a spectrofluorimeter. Such fluorescence, taken as an indication of intracellular calcium ion concentration ([Ca2+]i), increased as exogenous calcium ion concentration ([Ca2+]o) was raised to 1 mM. At [Ca2+]o approximately equal to 10 microM, [Ca2+]i = 72 +/- 14 nM (n = 26); at [Ca2+]o = 1 mM, [Ca2+]i = 140-220 nM, levels not increased by N, N, N', N'-tetrakis (2-pyridylmethyl) ethylenediamine, a membrane-permeant chelator of heavy metals than can quench quin2. Addition of mouse alpha + beta fibroblast interferon, lipopolysaccharide, thrombin, collagen, vasopressin, ADP, compound 48/80, or U46619 did not change [Ca2+]i. However, addition of platelet activating factor (PAF) (2-20 ng/ml) raised [Ca2+]i by 480 nM within 1 min if [Ca2+]o = 1 mM. In the presence of 5 mM EGTA, PAF raised [Ca2+]i by 25 nM. This suggests that PAF causes influx of exogenous Ca2+, as well as releasing some Ca2+ from intracellular stores. Consistent with these results, when PAF was added to 1 mM Ca2+ in the presence of 100 microM Cd2+ or Mn2+ to block Ca2+ influx, [Ca2+]i increased by only intermediate amounts; at the times of such dampened peak response, [Ca2+]i could be raised within 1 min to normal PAF-stimulated levels by chelation of the exogenous heavy metals with diethylenetriaminepentaacetic acid. Normal PAF responses were observed in the presence of indomethacin. The lowest dose of PAF observed to raise [Ca2+]i was 0.1 ng/ml. Response of [Ca2+]i to 2-20 ng/ml PAF was transient, and second applications had no effect. The PAF response also was seen in cell suspensions. These results suggest that an increase in [Ca2+]i may be an early event in PAF activation of macrophages.
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PMID:Platelet activating factor raises intracellular calcium ion concentration in macrophages. 373 74

In order to elucidate the mechanism(s) responsible for the prolonged antidiuretic activity of 1-deamino-[8-D-arginine]-vasopressin (dDAVP), antidiuretic activities of dDAVP and arginine vasopressin (AVP) were determined in the rat following either oral administration or incubation with AVP-degrading enzymes and reagents. Oral administration of dDAVP to conscious water-loaded rats resulted in significant antidiuresis while AVP resulted in slight and transient antidiuresis. In the ethanol anesthetized water-loaded rats, antidiuretic activities of 136pg of AVP and 50pg of dDAVP, which were found to be equipotent, were compared after incubation with digestive enzymes (pepsin, trypsin, alpha-chymotrypsin), late pregnancy plasma, or sodium thioglycollate. The antidiuretic activity of AVP was completely destroyed by 30-min incubation with trypsin, alpha-chymotrypsin, or late pregnancy plasma and almost all AVP was inactivated by 0.2 M sodium thioglycollate. On the other hand, the antidiuretic activity of dDAVP was not destroyed by trypsin or pregnancy plasma but was partly destroyed by alpha-chymotrypsin and sodium thioglycollate. Neither the antidiuretic activity of AVP nor that of dDAVP was affected by pepsin. Thus, the antidiuresis observed after oral administration of dDAVP might be brought about by the resistance to digestive enzymes. Furthermore, the resistance of dDAVP to digestive enzymes, late pregnancy plasma and sodium thioglycollate might be responsible for the prolonged antidiuretic action of dDAVP in vivo.
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PMID:Resistance of 1-deamino-[8-D-arginine]-vasopressin to in vitro degradation as compared with arginine vasopressin. 393 2

Identifying posterior pituitary hormones in body fluids or neurohypophysial extracts was heretofore partially achieved by using pharmacologic potency ratios or semispecific inactivation by thioglycolate or enzymes. Production of antisera against oxytocin and lysine-vasopressin has prompted us to test their specificity against lysine-vasopressin, arginine-vasopressin, arginine-vasotocin, and oxytocin. In ethanol anesthetized rats, antidiuretic and milk-ejection activities were assayed for each peptide-antiserum combination after 0, 30, 60, and 90 min of incubation. Results indicate that (a) oxytocin antiserum inactivates oxytocin, but not arginine-vasopressin, lysine-vasopressin, or arginine-vasotocin; vasopressin antiserum inactivates arginine-vasopressin and lysine-vasopressin, but neither oxytocin nor arginine-vasotocin; (b) an identifiable antigenic site exists for each hormone; (c) relatively specific identifications of natural neurohypophysial peptides are possible using antisera and bioassays; (d) this method is promising for identifying neurohypophysial peptides in body fluids and pituitary extracts; and (e) active and passive immunization against oxytocin and vasopressin may increase our understanding of their physiologic functions.
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PMID:Identification of neurohypophysial hormones with their antisera. 544 83

1. Isolated hearts release a steroid-like substance into the blood stream when venous return is decreased. This substance very closely resembles the 18 monoacetate of D-aldosterone (18 MA) in physicochemical and biological properties.2. Hence the changes in the flow and composition of the urine caused by infusions of the 18 MA have been examined in cats.3. The threshold effect of both 18 MA and of antidiuretic hormone (ADH) may be antidiuretic, but higher concentrations of both substances usually produce diuresis in cats under chloralose anaesthesia.4. Both ADH and 18 MA are antidiuretic in decerebrate cats.5. In decerebrate cats and in cats under chloralose anaesthesia the renal actions of 18 MA, 0.003-0.02 mug/kg.min are abolished by hypophysectomy: responses to ADH remain unchanged.6. 18 MA, 0.012 mug/kg.min causes the appearance of thioglycollate labile antidiuretic activity in blood taken from the terminal descending portion of the left lateral sinus.7. 18 MA, 0.05-0.15 mug/kg.min causes diuresis followed by antidiuresis in cats under chloralose anaesthesia. Hypophysectomy abolishes the diuretic phase of the response and uncovers the short latency of the antidiuretic. The antidiuresis is accompanied by reduction in the concentration of urinary Na and a fall in the ratio Na/K of the urine.
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PMID:Changes in the flow and composition of the urine induced by the 18 monoacetate of D-aldosterone, in cats. 578 43

1. An oxytocic substance has been isolated from ox hypothalamus by successive gel filtration on Sephadex G-25 and Sephadex G-50, and its pharmacology has been examined on three smooth muscle preparations.2. The substance has the same order of potency on rat uterus, guinea-pig ileum, and hen rectal caecum.3. The action of the substance on rat uterus was not abolished by thioglycollate.4. Atropine (1.0 mug/ml.), phenoxybenzamine (0.1 mug/ml.) and mepyramine (1.0 mug/ml.) did not block the smooth muscle action of the substance.5. Drug action, relative potency, and log dose-response relationships distinguish the substance from 5-hydroxytryptamine, acetylcholine, oxytocin, vasopressin, angiotensin amide, bradykinin, and purified preparations of substance P.
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PMID:The pharmacology of a new oxytocic principle from ox hypothalamus. 581 85

Electrical stimulation of rat posterior lobes in vitro inhibited bioactive corticotropin (ACTH) release from the intermediate lobe and promoted the release of corticotropin-releasing factor(s) (CRF). Both effects were calcium dependent. Released posterior lobe CRF was inactivated by thioglycolate, and the CRF activity could be accounted for by vasopressin. Results suggest strongly that vasopressin is the predominant CRF released from neurohypophysial axons, and that intermediate lobe ACTH release is submitted to an inhibitory control.
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PMID:Release of corticotropin and corticotropin-releasing factors from rat posterior pituitary in vitro. 624 58

In diabetes insipidus (DI) rats, electrical stimulation of the posterior pituitary lobes in vitro promotes the release of corticotropin-releasing factor (CRF). The CRF activity is abolished by preincubation of the posterior lobe media with thioglycolate. Oxytocin, which is released concomitantly into the medium (3.2 mIU/lobe/20 min), accounts for the complete CRF effect. Neural lobe extracts from DI and normal rats contain 40-70% more CRF activity than can be explained by their content in vasopressin and/or oxytocin. The discrepancy between released and extracted CRFs suggests that hypothetical CRFs or potentiating factors are not released from nerve endings or have to be present in high concentrations to manifest their effect.
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PMID:Oxytocin: major corticotropin-releasing factor secreted from diabetes insipidus rat posterior pituitary in vitro. 625 96

Stimulation of left atrial receptors causes a diuresis partly through a blood borne agent. Malpighian tubules of Rhodnius prolixus can detect a blood borne agent during the diuresis. It has been suggested that the agent is ADH but this is in dispute. In the present investigation, vasopressin (1-300 mu i.u. cm-3) was found to have no effect on Malpighian tubule secretion when added to plasma, Rhodnius Ringer and Rhodnius Ringer + 5-HT. In addition, it was shown that incubation with sodium thioglycollate of plasma samples obtained from anaesthetized dogs, before and during stimulation of atrial receptors by distension of a balloon in the lumen of the left atrium, did not abolish the differences between test and control plasma samples detected by the Malpighian tubules. It is concluded that differences in plasma detected by the Malpighian tubules and related to the diuresis which results from left atrial stimulation are not attributable to changes in concentration of ADH.
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PMID:Diuresis from stimulation of left atrial receptors: ADH and the Malpighian tubules of Rhodnius prolixus. 691 Jul 34

The plasma antidiuretic activity and the content of antidiuretic hormone (ADH) and oxytocin of the neurointermediate lobe were determined in male rats under normal conditions and after copulation. The plasma samples from control rats assayed directly in the water-loaded ethanol-anaesthetized rat had no detectable antidiuretic activity. The same negative result was observed in plasma obtained from male rats during courtship. However, plasma obtained from male rats at different time intervals after copulation had an antidiuretic activity which was maximal one h after ejaculation. When the ADH was extracted from pools of plasma samples, the circulating level of the hormone in control rats was also measured. The plasma antidiuretic activity after copulation was abolished after thioglycolate treatment which inactivates the neurohypophysial hormones. These findings suggest that ADH is released after copulation and that such a release is maintained for at lest 60 min.
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PMID:The effect of copulation on the plasma antidiuretic activity of the male rat. 706 57


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