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 age-dependent polydipsia and polyuria observed in SWR/J mice was found to be caused by relative inability of the kidneys to respond to antidiuretic hormone (ADH), resulting in a concentrating defect, which persisted even following Pitressin injection or water deprivation. Posterior pituitaries contained large amounts of ADH, which was also found in the urine and increased in output following water deprivation, indicating normal, or above normal synthesis and release of ADH. Kidneys of polydipsic SWR/J mice weighed more than those of normal strains and sometimes contained a lesion in the medullary area. No clear relationship was found between the size of the lesion and water intake.
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PMID:Renal deficiency associated with diabetes insipidus in the SWR/J mouse. 118 37

The aims of this study were: (1) to examine whether the posterior pituitary contains prolactin releasing factor (PRF) activity, (2) to determine to what extent known neurohypophyseal peptides contribute to this activity, and (3) to compare posterior pituitary PRF activities of hens in different reproductive stages. Anterior pituitary cells derived from juvenile female turkeys were incubated with posterior pituitary extracts or test substances for 3 hr. Posterior pituitary extracts (0.1-0.8 equivalent) contained a potent substance(s) which stimulated PRL release in a concentration-dependent manner (2.4 +/- 0.08 to 6.5 +/- 0.23 micrograms/500 k cells). Arginine vasotocin (AVT) and vasoactive intestinal peptide (VIP) antisera (1:500) completely abolished the PRL-releasing activities of their respective peptides but partially reduced (P less than 0.05) the PRF activity of the posterior pituitary (AVT, 19.9%; VIP, 55.1%). Mesotocin antiserum did not alter (P greater than 0.05) PRL release induced by posterior pituitary extract. Posterior pituitary extract (0.01-0.5 equivalent) from hens in each of the various stages of the reproductive cycle induced a concentration dependent PRL release. The 0.5 posterior pituitary equivalent dose from reproductively quiescent (nonphotostimulated), laying, photorefractory, and incubating hens increased PRL release 2.4-, 2.9-, 3.8-, and 11.1-fold, respectively. The turkey posterior pituitary contains a potent PRF activity, partially accounted for by VIP and AVT, at the assayed concentrations, which varies with the reproductive cycle.
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PMID:Evidence of a role for the turkey posterior pituitary in prolactin release. 142 46

Preliminary studies in rats (COSMOS 1887) suggested that levels of posterior pituitary hormones were reduced by exposure to spaceflight. To confirm these preliminary findings, we obtained pituitary tissue from rats flown for 14 days on COSMOS 2044. Posterior pituitary content of oxytocin (OT) and vasopressin (VP) were measured in these tissues as well as those from ground-based controls. The synchronous control group had feeding and lighting schedules synchronized to those in the spacecraft and were maintained in flight-type cages. Another group was housed in vivarium cages; a third group was tail suspended (T), a method used to stimulate microgravity. Flight rats showed an average reduction of 27% (P less than 0.05) in pituitary OT and VP compared with the three control groups. When hormone content was expressed in terms of pituitary protein (micrograms hormone/mg protein), the average decrease in OT and VP for the flight animals ranged from 20 to 33% (P less than 0.05) compared with the various control groups. Reduced levels of pituitary OT and VP were similar to preliminary measurements from the COSMOS 1887 mission and appear to result from exposure to spaceflight. These data suggest that changes in the rate of hormone secretion or synthesis may have occurred during exposure to microgravity.
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PMID:Pituitary oxytocin and vasopressin content of rats flown on COSMOS 2044. 152 46

We have recently reported that the posterior pituitary contains PRL-releasing factor (PRF), a small (less than 5000 mol wt) peptide which induces a rapid, hormone-specific, and concentration-dependent stimulation of PRL secretion. Although the identity of posterior pituitary PRF is yet unknown, it is distinct from known PRL secretagogues. Recently, the vasopressin-associated glycopeptide (VAG), which is concentrated in the posterior pituitary, was suggested as a PRF. To investigate whether VAG functions as a PRF, we used Brattleboro rats, which are deficient in arginine vasopressin (AVP), AVP-associated neurophysin, and VAG. Homozygous (DI) and heterozygous (HZ) lactating Brattleboro rats were used. The water consumption of pregnant DI rats (greater than 300 ml/day) was 6-fold higher than that of HZ rats. To correct their water imbalance, DI rats were implanted with osmotic minipumps containing the vasopressin analog 1-desamino-8-D-arginine vasopressin. On days 7-8 of lactation, pups were separated for 6 h, and blood was collected from the dams via a jugular cannula. Upon introduction of the pups, plasma PRL levels increased 100-fold in both DI and HZ rats and remained elevated for the duration of suckling. The suckling-induced rises in plasma oxytocin in DI and HZ rats were also superimposable. The weight gains of the pups of DI and HZ mothers were similar. PRF activity was determined using perifused anterior pituitary cells. Posterior pituitaries from DI and HZ rats contained equivalent amounts of PRF activity. Moreover, purified rat VAG (1.5 and 6.0 micrograms) failed to stimulate PRL release from pituitary cells. The posterior pituitary content of immunoreactive AVP was 2500-fold higher in HZ rats, but the contents of dopamine and oxytocin were similar. It is concluded that VAG neither mediates the suckling-induced rise of plasma PRL, nor stimulates PRL secretion from perifused anterior pituitary cells. Furthermore, posterior pituitaries from DI and HZ rats contain equivalent amounts of PRF activity. Collectively, these data indicate that VAG is not the posterior pituitary PRF.
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PMID:The vasopressin-associated glycopeptide is not a prolactin-releasing factor: studies with lactating Brattleboro rats. 250 Mar 28

In order to determine if the decreased hypothalamic and increased posterior pituitary content of vasopressin (VP) observed previously in spontaneously hypertensive rats (SHR) were a secondary consequence of the hypertension, the effect of preventing the development of hypertension on VP content of the hypothalamoneurohypophyseal system was evaluated. Two methods for preventing the hypertension were used: (1) chronic angiotensin-converting enzyme inhibition (oral captopril, 100 mg/kg/day at 4-12 weeks of age); and (2) intraventricular 6-hydroxydopamine (6-OHDA, 200 micrograms at 4 and 5 weeks of age). Both of these treatments markedly attenuated the increase in systolic blood pressure in SHRs at 5-11 weeks of age. The captopril-treated rats had a significant elevation in serum renin activity at 12 weeks of age indicating the presence of chronic converting enzyme inhibition, and the 6-OHDA-treatment resulted in a depletion of hypothalamic (86%) and brainstem (76%) norepinephrine content. Hypothalamic VP content was reduced in untreated SHRs compared to normotensive Wistar-Kyoto rats (WKYs, P = 0.0015). It was not significantly altered in either strain by the 6-OHDA treatment. Captopril caused a reduction in hypothalamic VP content in both SHRs and WKYs (P less than 0.01). Posterior pituitary VP content was elevated in untreated SHRs compared to WKYs (P less than 0.001), and remained elevated with captopril and 6-OHDA treatments. These data indicate that the abnormalities in VP content in the hypothalamus and posterior pituitary of SHRs are not a response to the hypertension. Therefore, they may represent primary abnormalities in the SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormalities in hypothalamic and neurohypophysial vasopressin content are not a consequence of hypertension in the spontaneously hypertensive rat. 313 Jan 52

Hypernatremia has occasionally been observed in patients with myotonic muscular dystrophy (MyD). To elucidate the possibility of osmoregulatory dysfunction, we investigated hypothalamo-posterior pituitary function as well as serum electrolytes in eight patients with MyD. Blood samples were obtained early in the morning after overnight dehydration. Renal function was estimated by blood urea nitrogen, serum creatinine and creatinine clearance. Posterior pituitary function was evaluated by direct measurement of plasma vasopressin (AVP) during a 5% hypertonic saline infusion. Plasma AVP concentrations were determined by sensitive radioimmunoassay. In five patients, circulating blood volume (CBV), plasma renin activity (PRA) and serum aldosterone (S-Aldo.) were also measured. The mean serum sodium level (143.9 +/- 1.7mEq/1: Mean +/- SD) was significantly higher than in the controls (139.4 +/- 2.2mEq/1). A 5% hypertonic saline infusion showed a subnormal increase in AVP and diminished thirst, despite sufficient elevation of plasma osmolality, in all patients as compared with healthy adults. Renal function was intact. Biochemical evidence of dehydration, estimated by PRA, S-Aldo and CBV, was unremarkable in four of the five patients. These findings suggest that patients with MyD have neurogenic disorders of osmoregulation in addition to previously reported endocrine abnormalities. Impaired AVP secretion in response to osmotic stimuli and reduced thirst might be responsible for such failure.
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PMID:[Impaired vasopressin secretion in patients with myotonic dystrophy]. 328 99

Posterior pituitary injection is an extract prepared from the dried posterior lobe of the pituitary gland from domestic animals containing two octapeptide hormones, oxytocin and vasopressin. Posterior pituitary injection carries an approved therapeutic indication as an adjunct measure for achieving surgical hemostasis. We report a case of cerebral edema and death attributed to water intoxication in a child who had received a large volume of free water concurrent with posterior pituitary injection to control bleeding after tonsillectomy and adenoidectomy.
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PMID:Water intoxication and death associated with the use of posterior pituitary injection for surgical hemostasis. 372 May 41

Seven mouse monoclonal antibodies (IgGs) were produced against rat neurophysins (NPs). Three were specifically directed against vasopressin-associated NP (NP-AVP), and four were specific for oxytocin-associated NP (NP-OT). These specificities were observed in liquid phase assays, immunoblot, and immunoprecipitation experiments. Homozygous Brattleboro rat tissues and extracts, which do not contain vasopressin or NP-AVP, did not react with the anti-NP-AVP antibodies but reacted with high affinity to the anti-NP-OT antibodies. In immunoprecipitation assays the antibodies brought down the appropriate NPs as well as their precursor molecules synthesized in vivo with no detectable cross-reactivity. In solid phase assays where the antigens were presented in a different manner, there was a significant cross-reactivity of the anti-NP-AVP antibodies with NP-OT. The extent of this cross-reactivity in solid phase correlated with the cross-reactivities of the antibodies observed in immunocytochemical studies. These solid phase (and immunocytochemical) data demonstrated that liquid phase specificities and absorption controls of antibodies are inadequate to assess their immunocytochemical (solid phase) specificities. Posterior pituitary extracts from the mouse and frog, as well as purified NPs from the rat, cow, and human were studied for their cross-reactivities to two of the antibodies, PS 36 and PS 45. In liquid phase assays the anti-rat NP-OT antibody, PS 36, reacted only with rat and mouse NPs and did not cross-react with NPs from any of the other species. In contrast, the anti-rat NP-AVP antibody, PS 45, was cross-reactive across species lines including an NP-like antigen extracted from frog posterior pituitaries. Immunoblot staining with these antibodies showed heterogeneity of NP-AVP and NP-OT in the rat posterior pituitary. Analysis of the epitopes for PS 36 and PS 45 indicated the antigenic determinants were located near amino acid positions 80 to 81 in NP-OT and 75 to 86 in NP-AVP, respectively.
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PMID:Neurophysin in the hypothalamo-neurohypophysial system. I. Production and characterization of monoclonal antibodies. 388 Aug 13

Hormonal disturbances caused by hypothalamic pathology can be treated effectively by target hormone replacement in the case of failure of glandotropic hormone secretion. Hyposomatotropism in children has to be substituted by parenteral administration of growth hormone. In addition gonadotropins respectively gonadotropin releasing factor have to be given in order to restore fertility in hypothalamic hypogonadism. Posterior pituitary failure can be adequately replaced by administration of analogues of antidiuretic hormone. Hypothalamic pathology causing hypersecretion of anterior pituitary hormones may also be accessable to medical treatment. This pertains particularly to hyperprolactinemia and precocious puberty. However, there is no medical therapy so far for hypothalamic disturbances leading to veterative dysfunction like disturbances of temperature regulation and control of thirst and polyphagia. In this situation symptomatic correction of the abnormality represents the only possibility to keep these patients alive.
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PMID:Medical therapy of hypothalamic diseases. 399 50

Ultrastructural and electrophysiological studies of the rat neurohypophysis was carried out following stimulation to cause vasopressin release. Unit activity was investigated with microelectrodes, filtered, integrated, and recorded simultaneously with blood pressure in a polygraph. The basal unit activity was challenged by perfusing the hypothalamus and pituitary gland with hypertonic, hypotonic, and isotonic solutions through the internal carotid and by bleeding. Posterior lobes were fixed in osmium tetroxide and stained with uranyl acetate for electron microscopy. Single unit activity from the neural lobe showed mostly a continuous pattern of activity with a rate of discharge (RD) of 7 to 30 pulses per 10 s during control periods. Following hypertonic stimulation, out of 20 units studied, 35% increased, 10% decreased, and 55% did not change their RD. The effect of bleeding was studied in 34 units. Following the withdrawal of 1 ml of blood from the jugular vein, 29% increased, 32% decreased, and 38% did not change their RD. It is concluded that the existence in the neurohypophysis of fibers which are excited or inhibited by stimuli known to cause vasopressin release supports the hypothesis of the existence of a modulatory mechanism for neuropeptide release in the neural lobe.
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PMID:Ultrastructure and electrical activity of the rat neurohypophysis. 406 45


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