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)

Various fractions were tested in vivo for corticotropin-releasing factor (CRF) activity after Sephadex G-100 fractionation of 0.1-N HCl extracts of bovine hypophyseal stalk or cerebral cortex. Female rats pretreated with chlorpromazine, morphine, and Nembutal were used for CRF assay. CRF-A (void volume fractions; big CRF), CRF-B (Kav = 0.583), and CRF-C (salt volume fractions) of bovine hypophyseal stalk and lysine or arginine vasopressin all induced clear-cut stimulation of ACTH and corticosterone in the assay rat, whereas they were ineffective in acutely hypophysectomized rats. Control fractions purified from bovine cerebral cortex had no CRF activity. Treatment of arginine and lysine vasopressin and CRF-C with dithiothreitol and iodoacetamide completely abolished their CRF activity, whereas the CRF activities of CRF-A and CRF-B were unaltered by these treatments. Treatment with iodoacetamide alone had no effect on the CRF activity of any of these substances. Fractionation of either CRF-C or arginine vasopressin on Sephadex G-15 yielded a CRF-active peak at a Kav of 0.35. We conclude that 1) three different forms of CRF exist in bovine hypophyseal stalk; 2) CRF-A and CRF-B are unrelated to vasopressin and require neither a disulfide bond(s) nor a sulfhydryl group(s) for their CRF activity; 3) reduction of the disulfide bond of vasopressin destroys both CRF and antidiuretic activities; 4) CRF-C requires an intact disulfide bond(s) for its CRF activity and is likely to be either vasopressin itself or a substance closely related to vasopressin; and 5) CRF-B is likely to be the physiologically important form of bovine CRF.
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PMID:Differential effects of dithiothreitol and iodoacetamide on corticotropin-releasing factor (CRF) activity of bovine hypothalamic CRFs and vasopressin. 628 Sep 87

The i.v. bolus of 50 ng kg-1 Arginine-vasopressin administered to adult male rats anaesthetized with Pentobarbital (50 mg kg-1 i.p.) increases the activity of liver glycogen phosphorylase in fed and 24 h fasted rats to the same extent; after 25 ng kg-1 of the drug the enzyme response after fasting is barely detectable, whereas in the fed animals a response similar to that after 50 ng kg-1 persists.
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PMID:Inhibitory effect of fasting on the activation of liver glycogen phosphorylase of rats by arginine-vasopressin. 631 93

The biological activity of partially purified bovine hypothalamic CRF (corticotrophin- releasing factor) was compared to those of synthetic CRFs (ovine, rat) sauvagine and vasopressin in vivo and in vitro. ACTH-primed hypophysectomized rats with heterotopically transplanted pituitaries and medial basal hypothalamic ablation (H-T + MBHA ), and intact rats pre-treated with chlorpromazine, morphine and Nembutal (C-M-N) were used for in vivo CRF assays. Perifused rat adenohypophyseal fragments were employed for in vitro studies. CRF-A (void volume fractions, 'big' CRF) and CRF-B (Kav = 0.583) purified from bovine hypophyseal stalk, synthetic ovine and rat CRF, and sauvagine all induced significant stimulation of ACTH and/or corticosterone secretion in these systems. Synthetic ovine and rat CRF and sauvagine showed comparable CRF potency. The CRF dose-response slopes for bovine CRF were somewhat steeper than those for ovine CRF or sauvagine in the in vitro system. Vasopressin had the least steep dose-response slope. Intravenous bolus administration of ovine CRF caused a more prolonged (greater than 20 min) elevation of plasma ACTH compared to a relatively short duration after bovine CRF-A. These data suggest that bovine hypothalamus contains substance(s) which exhibits different CRF characteristics from those of ovine CRF.
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PMID:In vivo and in vitro comparisons of biological activities of bovine, ovine and rat CRF (corticotrophin-releasing factor). 632 21

Histamine increased vasopressin levels, as measured by radioimmunoassay (RIA), in both cerebrospinal fluid (CSF) and plasma of hypophysectomized rats, while histamine enhanced plasma but not CSF levels of vasopressin in sham operated rats. Pentobarbitone increased CSF vasopressin levels in hypophysectomized rats and in sham operated animals. The present data demonstrate that the histamine induced elevation of vasopressin levels in the blood is only temporarily disturbed after hypophysectomy, while the effect of histamine on CSF vasopressin levels of hypophysectomized rats is of a more permanent nature.
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PMID:Influence of histamine and pentobarbitone on plasma and CSF vasopressin levels of hypophysectomized rats. 711 2

The level of antidiuretic hormone (ADH) in the plasma of pigs was studied during hypozia, anaesthesia and a combination of the two conditions. Hypoxia, caused by making conscious pigs breathe nitrogen, elicited a rise in the level of ADH without change in plasma osmolality; the hypoxia was accompanied in some cases by a slight lowering of arterial pressure which quickly returned to its original level after the period of hypoxic breathing. Pentobarbitone anaesthesia had no significant effect on the level of ADH but halothane anaesthesia elicited a rise in ADH. Transient high levels of ADH were seen in animals which were exposed to hypoxia during halothane or pentobarbitone anaesthesia. These high levels of ADH were sometimes, but not invariably, accompanied by a fall in arterial pressure. No consistent changes in plasma osmolality or haematocrit were associated with the raised plasma ADH.
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PMID:Plasma antidiurectic hormone during hypoxia and anaesthesia in pigs. 740 Jul 13

Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O2 consumption (CMRO2) than in postnatal sheep. The fetus is exposed to a lower PO2. We tested the hypothesis that low PO2 in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMRO2. Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmHg] and hypoxic (14 +/- 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady-state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMRO2 were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO2 is unlikely to be the major mechanism for the potent Cushing response in the fetus.
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PMID:Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs. 823 67


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