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 effects of TRH upon neurohypophyseal hormone release were studied in conscious rabbits. Intravenous infusion of 250 nm/kg TRH had no significant effect on either arginine vasopressin (AVP) or oxytocin (OT) release, but a 5-fold greater dose led to significant increases in plasma levels of both AVP and OT and behavioral arousal. Intraventricular injection of 3 nm TRH produced significant elevations of both plasma AVP and OT, with even greater effects on behavior than after iv infusion. The maximal hormone response to intraventricular injection was observed considerably earlier than that for iv injection and the response occurred after an almost 1000-fold lower dose of TRH. Neither artificial cerebrospinal fluid vehicle nor the inactive analogue D-tyrosine2 TRH (p-Glu-d-Tyr-Proamide) had any effect on neurohypophyseal hormone release or on behavior. MK-771 [L-N-(2-oxopiperidin-6-YL-carbonyl)-L-histidyl-L-thiazolidine-4-carboxamide], a TRH analog with enhanced central nervous system effects, had effects on AVP and OT release comparable to equimolar doses of TRH. TRH stimulates release of both AVP and OT after both intraventricular and iv injection, and these effects may be independent of behavioral activation.
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PMID:Thyrotropin-releasing hormone stimulates release of arginine vasopressin and oxytocin in vivo. 10 88

An enzyme which catalyzes the deamidation of thyroliberin (TRF; less than Glu-His-Pro-NH2) has been purified 110-fold from extracts of bovine anterior pituitary by ammonium sulfate fractionation, ion exchange chromatography on DEAE-cellulose, and gel filtration. This enzyme of 76,000 molecular weight (as estimated by gel filtration) exhibits maximal activity at neutral pH (optimum pH 7.4 to 7.6) in buffers of high ionic strength supplemented with thiol-protecting agents. As indicated by the strong inhibition of the enzymatic activity by N-ethylmaleimide and Hg2+, as well as by the extreme sensitivity toward diisopropyl fluorophosphate, -SH, and -OH residues apparently represent essential functional groups of the enzyme. The stereospecific deamidation of TRF (Km = 4.1 . 10(-4) M) is inhibited competitively by TRF analogues which contain proline or by the proline containing biologically active peptides luliberin (LH-RF), oxytocin, vasopressin, angiotensin II, and Substance P. TRF analogues without proline or peptide amides without proline are ineffective. This enzyme cleaves the appropriate Pro-X bonds in luliberin, angiotensin II, pyroGlu-His-Pro-Gly-NH2, and the collagenase substrate Z-Gly-Pro-Leu-Gly-Pro. Thus, it may be characterized as a post-proline-cleaving enzyme.
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PMID:Characterization of "thyroliberin-deamidating enzyme" as a post-proline-cleaving enzyme. Partial purification and enzyme-chemical analysis of the enzyme from anterior pituitary tissue. 11 64

A continuous cell line was previously obtained by Simian Virus (SV) 40 transformation of primary cultures of dissociated mouse fetal hypothalami. One clone from this cell line has been previously shown to possess some of the ultrastructural features, immunological properties and synthesizing capacities of magnocellular hypothalamic neurons which secrete vasopressin and neurophysins. The present paper reports on the morphological characterization of 14 other clones or subclones of the original cell line, using the following criteria: phase contrast microscopy, electron microscopy, Gomori's aldehyde fuchsin staining, cytochemical detection of beta-glucuronidase, immunochemical staining with antisera against bovine neurophysin I, bovine neurophysin II, lys-vasopressin, oxytocin, LH-RH and TRH. The results allowed the conclusion that the clones as well as the subclones can be distributed into two groups: 1) neurosecretory neurons which all possess several of the ultrastructural and cytochemical features of the neurophysin-vasopressin synthesizing clone, and 2) primitive nerve cells which are devoid of such features but display numerous bundles of filaments. In addition some clones were found to display intermediate features between groups 1 and 2. A similar diversity was observed within clones of the original strain and subclones of a neurosecretory clone. It is suggested that the primitive clones could represent precursors of the neurosecretory clones.
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PMID:Ultrastructural and cytochemical features of SV 40 transformed hypothalamic cell lines. 18 90

Several procedures have been reported for the assay of corticotrophine-releasing factor (CRF), each having its advantages and disadvantages. This report deals with an in vitro assay of ACTH releasing activity utilizing pituitary incubation combined with ACTH radioimmunoassay. Rat half pituitary was preincubated in 2 ml Krebs Ringer bicarbonate buffer containing 0.2% glucose and 0.25 % BSA (KRBG-BSA) for 1.5 hr (45 min X 2). The medium was replaced by 1 ml KRBG-BSA and incubated for 30 min. Then the medium was again replaced by 1 ml KRBG-BSA or KRBG-BSA containing test materials and incubated for another 30 min. The amount of ACTH assayed by radioimmunoassay in the 2nd 30 min incubation was compared with in the 1st 30 min incubation and expressed as percentage. In ACTH radioimmunoassay, anti-ACTH serum was diluted to 1 : 1,500-3,000. The 125I-alpha 1-24ACTH-antibody system was not affected by lysine-vasopressin (LVP), arginine-vasopressin (AVP), rat's pituitary LH, GH and prolactin. Human 1-39ACTH was used as ACTH standard, and the dilution curve of incubation medium was paralleled with the standard curve. Repeatability of immunoassayable ACTH within-assay was 174 +/- 5.0 pg/tube (CV = 2.9%). A log dose-relationship was observed between the amounts of stalk median eminence extracts (SME ; NIAMDD) added to the incubation medium and its ACTH releasing activities. The sensitivity of this assay method was at least 0.1 SME or 10 mU of LVP and AVP. Using this method, it found that LVP, AVP, norepinephrine (100 ng/ml200 ng/ml) and 5-hydroxytryptophane (1 mug/ml) had ACTH releasing activities but LH-RH, TRH, glucagon, dopamine, phentolamine, propranolol, haloperidol, prostaglandin E1 and indomethacin did not affect the release of ACTH.
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PMID:[In vitro assay for ACTH-releasing activity using ACTH radioimmunoassay: ACTH releasing activities by various drugs (author's transl)]. 18 1

A patient with hypoadrenocorticism was found to have low basal plasma concentrations of ACTH and lipotropins and deficient responses of these hormones to insulin-induced hypoglycemia and lysine vasopressin. The adequacy of secretion of other anterior pituitary hormones was assessed either directly, by measuring their concentration in plasma, or indirectly, by assessing end organ function, under basal and stimulated conditions. The responses of gonadotropins to LRH and of PRL and TSH to TRH were normal. The etiology of this rare condition of isolated deficiency of ACTH and lipotropins remains to be elucidated.
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PMID:Isolated deficiency of adrenocorticotropin (ACTH) and lipotropins (LPHs). 23 63

Growth hormone-releasing hormone (GH-RH) activity in Sephadex G-25 fractions of porcine stalk median eminence (SME) extracts was examined in vivo by infusing these samples into a rat hypophyseal portal vessel. The increment of immunoreactive GH levels in the serum was used as the index for GH-RH activity. The GH-RH activities were found in two different locations: in the early fractions Nos. 3-4, and in somewhat retarded fraction No. 7. These GH-RH activities were not due to TRH, vasopressin, or potassium. The location of LH releasing hormone (LH-RH) and prolactin release-inhibiting hormone (PR-IH) determined in this in vivo system was in agreement with those found in other in vivo and in vitro assay systems for LH-RH and PR-IH, respectively. These results help validate this assay system.
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PMID:Assessment of GH releasing hormone activity in sephadex-separated fractions of porcine hypothalamic extracts by hypophyseal portal vessel infusion in the rat. 23 86

Pre- and postoperative evaluation of hypothalamic-pituitary function was performed in six children, aged 5.5 to 13.3 years with craniopharyngiomas. Before surgery growth hormone deficiency (GHD) was documented in four, hypothalamic hypothyroidism in three, and secondary ACTH-deficiency and hyperprolactinaemia in one patient. Diabetes insipidus was absent in all patients. After neurosurgical treatment GHD was present in all, hypothyroidism in five, ACTH-deficiency in three, hyperprolactinaemia in three, and diabetes insipidus in four children. The study shows that all endocrine functions tested may be defective even before surgery, although diabetes insipidus seems to be a rare preoperative complaint. Surgical intervention, however, often leads to additional endocrine disorders. From the data presented here one may suggest that TRH stimulation tests, evaluation of serum prolactin, and lysin-vasopressin stimulation tests are the most useful investigations to distinguish between hypothalamic and primary pituitary disorders.
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PMID:Pre- and postoperative evaluation of hypothalamo- pituitary function in children with craniopharyngiomas. 42 59

The rate of hydrolysis of several aminoacyl-4-nitroanilides by rat hypothalamic arylamidases was investigated. The activity of these enzymes which were mainly found in the 105 000 times g supernatant fraction of homogenates of the hypothalamus and other parts of the brain was shown to depend upon the presence of metal ions and free thiol groups, and to be inhibited by puromycin. As previous investigations had shown that Cys-NA is an appropiate substrate for measuring hormone effects on hypothalamic arylamidases, L-cystine arylamidase and its interaction with various peptide hormones were examined in detail. It could conclusively be shown that this enzyme interacts particularly with oligopeptides. Its activity was competitively inhibited by TRF, oxytocin, lysine vasopressin, and LH-RH. It was also shown that the biological activity of LH-RH and its inhibitory effect on the hydrolysis of L-cystine-bis-p-nitroanilide decreased when it was incubated for various periods of time with the 105 000 times g supernatant of rat hypothalumus homogenate.
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PMID:Inactivation of luteinizing hormone releasing hormone by rat hypothalamic L-cystine arylamidase. 80 61

A sensitive and specific radioimmunoassay has been developed capable of measuring thyrotropin releasing hormone (TRH) in extracted human plasma and urine. All of three TRH analogues tested had little cross-reactivity to antibody. Luteinizing hormone releasing hormone, lysine vasopressin, rat growth hormone and bovine albumin were without effect, but rat hypothalamic extract produced a displacement curve which was parallel to that obtained with the synthetic TRH. Sensitivity of the radioimmunoassay was 4 pg per tube with intraassay coefficient of variation of 6.2-9.7%. Synthetic TRH could be quantitatively extracted by methanol when added to human plasma in concentration of 25, 50 and 100 pg/ml. TRH immunoreactivity was rapidly reduced in plasma at 20 degrees C than at 0 degrees C, but addition of peptidase inhibitors, FOY-007 and BAL, prevented the inactivation of TRH for 3 hr at 0 degrees C. The TRH in urine was more stable at 0 degrees C than 20 degrees C, and recovered 75 +/- 4.6% hr after being added. The plasma levels of TRH were 19 pg/ml or less in normal adults and no sex difference was observed. The rate of disappearance of TRH administered i.v. from the blood could be represented as half-times of 4-12 min. Between 5.3-12.3% of the injected dose was excreted into urine within 1 hr as an immunoreactive TRH. These results indicate the usefulness of TRH radioimmunoassay for clinical investigation.
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PMID:Radioimmunoassay of thyrotropin releasing hormone in plasma and urine. 81 57

The reaction products of plasma enzyme degradation of TRH were identified by thin layer chromatography. The enzyme in normal rat plasma yields proline and pGlu-His as major reaction products. High concentrations of proline decrease peptide cleavage, resulting in greater amounts of acid TRH. The apparent Km of the enzyme is 4.1 X 10(-6) M. LHRH and neurotensin are competitive inhibitors with Ki of 5 X 10(-6) M and 1.5 X 10(-5) M, respectively. Somatostatin, MIF, oxytocin, arg-vasopressin, arg-vasotocin, neurophysin II and glucagon do not compete; and pGlu-His-Pro-OH, Glu-His-Pro-OH, pGlu-His, His-Pro-NH2, and Pro-NH2 do not affect enzyme activity. These data suggest that the substrated requires pGlu and a terminal or internal amide to complex with the enzyme. The enzyme is markedly inhibited by Cu++, Bal, benzamadine, p-(chloromercuri)-benzoic acid, moderately affected by EDTA and puromycin, and unaffected by mercaptoethanol. TSH does not affect enzyme activity while LH inhibits it moderately at high concentrations (300-600 pg/ml).
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PMID:Characteristics of the plasma TRH-degrading enzyme. 81 19


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