UNIPROT:P01185 - FACTA Search

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

Male Wistar rats received two i.p. injections of morphine-HCl, 2.5 mg/kg at 8.00 a.m. and 2.00 p.m. on the 1st day: the dose was doubled every other day to reach a total daily dose of 40 mg/kg on the 4th day. This schedule was maintained for 12 days. On day 16 the animals received the last injection of morphine, 20 mg/kg. One hour later (9.00 a.m.) six rats were decapitated and PRA, PAC and ACTH were measured by radioimmunoassay. Groups of six rats were killed at 9.00 a.m. on the 1st, 2nd, 5th and the 8th day after morphine withdrawal. Control data for PRA, PAC and ACTH were obtained from eighteen saline-injected rats. Nine out of morphine-treated animals were kept in metabolism cages to investigate simultaneously food and water intake. and renal excretion. Morphine withdrawal after chronic morphine treatment in the rat resulted in antidiuresis and a reduction of electrolyte excretion which were not due to a reduction in water and food intake. The simultaneous increase of PRA and PAC associated with decreased electrolyte excretion indicates that, in addition to antidiuretic hormone, also the renin-aldosterone-system probably play a relevant role in the renal excretory changes after morphine withdrawal.
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PMID:Effect of morphine withdrawal on food and water intake, urine output and electrolyte excretion in the rat: participation of the renin-aldosterone-system in renal excretory changes. 633 Oct 67

The subfornical organ (SFO), one of the brain circumventricular organs, contains immuno-reactive arginine-vasopressin (AVP). AVP in the SFO area may originate in neurons of the hypothalamo-neurohypophysial system. If AVP in the SFO area is part of the magnocellular neuroendocrine system and is important in the regulation of hydration, then its concentration [(]) should change during prolonged dehydration. The SFO is also a target for angiotensin II when the peptide stimulates drinking and releases AVP from the hypothalamo-neurohypophysial system. For these reasons, it was reasoned that hormones of the renin-angiotensin system may also influence [AVP] in the SFO area. To test these hypotheses [AVP] was measured in the SFO area, hippocampal commissure-fornix (HC-F), neural lobe and plasma of rats after 24, 48 and 72 h of water deprivation and at various times after intracerebroventricular (i.v.t.) administration of 5 milli -Goldblatt Units of renin. Before examining the responsiveness of [AVP] in these brain regions to stimulation, we characterized the extraction and recovery of AVP from brain tissue and determined the variance of [AVP] in the SFO area and HC-F among different groups of animals. AVP was extracted from pooled brain tissue into 0.1 N HCl. The homogenate was centrifuged and AVP in the supernatant was quantified by radioimmunoassay either directly or after bentonite extraction. AVP extracted from the SFO area and HC-F displaced labelled antigen bound to antisera in a manner similar to that displaced by standard AVP. The recovery of AVP, added to the 0.1 N HCl extract and assayed directly, averaged 78-108%, whereas 51% was recovered after bentonite extraction. [AVP] in the SFO area from 47 or more groups of 2-6 organs each, averaged 16 +/- 5 pg/organ, 16 +/- 4 pg/mg wet wt, 153 +/- 31 pg/mg protein, and was not significantly different from that contained in the HC-F, 10 +/- 1 pg/mg wet wt and 111 +/- 16 pg/mg protein. A frequency histogram of these data revealed a normal (HC-F) and skewed distribution (SFO). Water deprivation for 24, 48 and 72 h stimulated drinking and increased plasma [AVP]. The elevation in plasma [AVP] plateaued after 48 and 72 h of water deprivation, whereas [AVP] in the neural lobe was reduced (P less than 0.05). Water deprivation increased [AVP] in the HC-F (control vs 72 h water deprivation), but did not alter hormone in the SFO area when expressed as pg/mg protein or pg/mg wet wt.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of dehydration and renin on vasopressin concentration in the subfornical organ area. 637 9

To better characterize putative neurophysin-vasopressin prohormones in human posterior pituitary tissue, we extracted human posterior pituitary glands in 0.1 M HCl and isolated the higher molecular weight neurophysin-immunoreactive proteins. Sephadex G-75 gel filtration in 0.1 M formic acid with 6 M urea showed four distinct peaks of neurophysin immunoreactivity. Analysis of isolated lyophilized fractions of these peaks by sodium dodecyl sulfate-polyacrylamide gel electrophoresis revealed neurophysin-immunoreactive proteins at molecular weights of 10,000 daltons (79-87% of the total neurophysins), 19,000-20,000 daltons (10-16%), 26,000-30,000 daltons (1-2%), and a broad range of 30,000- to 100,000-dalton immunoreactivity from the void volume (V0) peak (2-3%). The 19,000- to 20,000-dalton and 26,000- to 30,000-dalton proteins were stable after both heating and treatment with reducing agents, but could be converted by chymotrypsin proteolysis to 10,000-dalton neurophysins and 3,000- to 5,000-dalton AVP-immunoreactive proteins. In contrast, the neurophysin immunoreactivity in the V0 peak was broken down to lower molecular weight neurophysin- and AVP-immunoreactive proteins by heating alone. Extraction of human posterior pituitaries in the presence of either [125I]human AVP-neurophysin or [35S] cysteine-labeled monkey neurophysin showed that no labeled neurophysin eluted in the areas of the 19,000- to 20,000- or 26,000- to 30,000-dalton proteins, but a significant fraction of the [35S]monkey neurophysin eluted in the V0. These data suggest that the 19,000- to 20,000- and 26,000- to 30,000-dalton human neurophysins represent stable proteins which are probably common precursor molecules for neurophysin and AVP, but the greater than 30,000-dalton neurophysins found in the V0 appear to be aggregates of neurophysins, neurophysin precursors, AVP, oxytocin, and probably other proteins and lipids as well, rather than very high molecular weight precursor proteins.
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PMID:Characterization of neurophysin-vasopressin prohormones in human posterior pituitary tissue. 640 29

Magnocellular neurons in the supraoptic and paraventricular nuclei synthesize and release vasopressin and oxytocin in response to dehydration. Pinealectomy has been observed to decrease the distribution in the supraoptic nuclei of thiamine diphosphate-phosphohydrolase, an enzyme specific for the Golgi apparatus that correlates positively with neurosecretory activity. Based upon these studies we postulated that pinealectomy would alter the concentration of neurohypohysial hormones in plasma elevated by 48 hr of water deprivation. In addition, we investigated the possibility that pinealectomy would affect vasopressin concentration in another circumventricular organ, the subfornical organ (SFO) and in a adjacent fiber tract of the limbic system, the hippocampal commissure-fornix (HC-F). Adult, male, Sprague-Dawley rats exposed to a 12 hr light/dark cycle were either unoperated (controls; C), sham-operated (Sham; S) or pinealectomized (PX) three weeks prior to testing. Food and water consumption and urinary excretion of Na and K were measured for 7 days. On the fifth day, half of the animals in each treatment group (C, S, PX) were deprived of water for 48 hr. Animals were decapitated on day 8. Vasopressin and oxytocin in plasma were extracted using bentonite and acetone-ether, respectively, then quantified by radioimmunoassay. The SFO and HC-F were microdissected from each brain. Like tissues from 4 rats were pooled, homogenized in 0.1 N HCl, and centrifuged. The supernatant was neutralized and vasopressin was quantified by radioimmunoassay. Dehydration resulted in antidiuresis, increased urine concentrations of Na and K, a decreased ratio of Na:K in urine, and reduced food consumption of similar magnitudes in all groups (C, S, PX; p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of pinealectomy on neurohypophysial hormones in the SFO and plasma of dehydrated rats exposed to 12 hours of light. 666 81

A 19-yr-old male developed severe hemorrhagic gastritis following three abdominal operations. Treatment with intravenous cimetidine and hourly antacids to maintain his gastric pH above 5 failed to affect gastrointestinal bleeding. Also, peripheral venous vasopressin, propantheline bromide, and glucagon were without effect. Total gastrectomy was considered to control his bleeding. However, since a number of prostaglandin analogs prevent gastric lesions produced by many noxious agents (e.g., aspirin, alcohol, strong acid or alkali, etc.) in animals and humans, the patient was treated with 50 micrograms of 15(R)-15 methyl prostaglandin E2 intragastrically every 6 h for 10 days. To epimerize the 15(R) form to the more active 15(S) form, 50-100 ml of 50-mN HCl was placed into the patient's stomach immediately before each dose. Bleeding ceased within 24 h of the onset of 15(R)-15 methyl prostaglandin E2 therapy and did not recur. The prompt response to 15(R)-15 methyl prostaglandin E2 in combination with hourly antacids in this patient with persistent and severe hemorrhagic gastritis suggests a therapeutic effect and the need for a prospective double-blind clinical trial.
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PMID:Treatment of hemorrhagic gastritis with 15(R)-15 methyl prostaglandin E2: report of a case. 697 84

Although prostacyclin (PGI2) causes an increase in resting gastric mucosal blood flow, this effect is not thought to be correlated with its cytoprotective action. This study questions that hypothesis by assessing whether PGI2 cytoprotection occurs in the presence of decreased gastric mucosal blood flow. Twenty-four miniature swine were anesthetized with chloralose, ventilated, and catheterized to measure cardiac output and arterial pressure and to inject microspheres. An orogastric tube was placed for infusion of 2.5% autogenous bile in isotonic HCl (2 ml/kg/hr). Four experimental groups were used: I, control (no drugs); II, vasopressin (0.25 U/min intravenously); III, PGI2 (0.1 micrograms/kg/min intravenously); and IV, vasopressin and PGI2 combined. Gastric mucosal blood flow was documented at baseline and at 1, 2, and 3 hours of drug infusion by radiolabeled-microsphere technique. Stomachs were harvested and photographed, and lesions were scored (0 to 3) by blinded observers. Gastric mucosal blood flow was decreased (50%) in both groups that received vasopressin, increased (300%) in animals that received PGI2 alone, and unchanged in controls. All animals that received vasopressin, whether alone or with PGI2, developed mucosal injury (mean score 2.5 versus (2.2). Group I and group III animals did not develop lesions. The results of this study demonstrate that PGI2 failed to elevate gastric mucosal blood flow, which was already depressed to vasopressin, and that PGI2 failed to protect the gastric mucosa from injury in the presence of reduced blood flow. This suggests that PGI2 cytoprotection is linked to its effect on gastric mucosal blood flow.
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PMID:Prostacyclin-mediated gastric cytoprotection is dependent on mucosal blood flow. 704 95

Proteins of the hypothalamo-neurohypophysial system of the rat were studied by means of a purpose-modified form of microelectrophoresis in the polyacrylamide gradient. The respective shares of neurophysins I, II and III in total neurophysin were found to be 58 +/- 16, 24 +/- 5 and 18 +/- 6% in HCl extracts and 48 +/- 7, 30 +/- 7 and 23 +/- 5% in aqueous extracts. In particular, neurophysin I was absent in homozygous Brattleboro rats, with no evidence being obtained as to aberrant neurophysins. Approximately equal neurophysin shares were observed for heterozygous Brattleboro rats. Using perfused material, one of the fractions occurring in neurohypophysial extracts was clearly identified as serum albumin. The electropherograms of aqueous neurohypophysial extracts revealed up to 43 protein fractions. Comparison with extracts from the median eminence, the nuclei of the hypothalamo-neurohyophysial system and other hypothalamic regions, as well as the results of incubation experiments distinguished one fraction as a possible candidate for the hitherto hypothetical neurophysin precursors. Incubation of neurohypophyses did not yield any signs of both conversion of neurophysin II into neurophysin III, and formation of further neurophysin derivatives.
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PMID:Identification and metabolic differentiation of rat neurophysins: a microelectrophoretic study. 737 4

The effect of barrier breakers on gastric mucosal blood flow (MBF) has been disputed, but the influence of acid back diffusion alone has never been studied. In anesthetized New Zealand white rabbits, intramural pH (pHi) and gastric MBF were measured with an antimony microelectrode and with radioactive microspheres (51Cr, 85Cr, 141Ce), respectively. Innervated fundic pouches were perfused with solutions of varying [H+] at 37 degrees C. In the rabbit, back flux of H+ is linearly dependent on luminal [H+] and in the present studies a direct positive linear correlation was found between luminal [H+] and MBF (r = 0.97 P < 0.001) while pHi remained unchanged up to luminal [H+] of 80 mM. The usual 80% increase in MBF induced by 80 mM HCl was prevented by pretreatment with vasopressin, which decreased pHi and caused gross ulceration. Without vasopressin, [H+] of 120 mM HCl produced gross mucosal ulceration and a decrease in MBF and pHi. Our data suggest that back diffusion of H+ influences MBF in the rabbit. There is an increasing MBF caused by increasing luminal [H+] up to 80 mM, beyond which MBF decreases. When the balance between back diffusion and MBF is disturbed by a vasoconstrictor or a high luminal [H+], pHi decreases and gross ulceration occurs.
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PMID:H+ back diffusion stimulating gastric mucosal blood flow in the rabbit fundus. 745 8

1. Acid back-diffusion through a disrupted gastric mucosal barrier increases blood flow to the stomach without any change in systemic blood pressure. This study was undertaken to examine the gastric acid-evoked changes in blood flow in a number of visceral and somatic arterial beds and to elucidate the mechanisms which lead to the regionally diverse haemodynamic responses. 2. The gastric mucosa of urethane-anaesthetized rats was challenged with acid by perfusing the stomach with ethanol (15%, to disrupt the gastric mucosal barrier) in 0.15 M HCl. Blood flow was estimated by laser Doppler flowmetry, the hydrogen clearance method or the ultrasonic transit time shift technique. 3. Gastric acid challenge increased blood flow in the gastric mucosa and left gastric artery while blood flow in the femoral artery and skin declined. 4. Afferent nerve stimulation by intragastric administration of capsaicin enhanced blood flow in the left gastric artery but did not diminish blood flow in the femoral artery when compared with the vehicle. 5. The gastric acid-evoked dilatation of the left gastric artery was depressed by acute extrinsic denervation of the stomach, capsaicin-induced ablation of afferent neurones or hexamethonium-induced blockade of autonomic ganglionic transmission. 6. The gastric acid-induced constriction of the femoral artery was attenuated by acute extrinsic denervation of the stomach but left unaltered by capsaicin, hexamethonium, guanethidine, indomethacin, telmisartan (an angiotensin II antagonist), [d(CH2)5(1), Tyr(Me)2, Arg8]-vasopressin (a vasopressin antagonist), bosentan (an endothelin antagonist) and acute ligation of the blood vessels to the adrenal glands. 7. These data show that acid challenge of the gastric mucosa elicits visceral vasodilatation and somatic vasoconstriction via divergent mechanisms. The gastric hyperaemia is brought about by extrinsic vasodilator nerves, whereas the reduction of somatic blood flow seems to be mediated by non-neural, probably humoral, vasoconstrictor messengers that remain to be identified.
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PMID:Visceral vasodilatation and somatic vasoconstriction evoked by acid challenge of the rat gastric mucosa: diversity of mechanisms. 747 14

Cardiovascular and sympathetic nervous system effects of the mixed alpha 2-adrenoceptor and imidazoline receptor agonist rilmenidine were studied in conscious rabbits chronically instrumented for the recording of the firing rate of renal sympathetic fibers. Separate experiments were carried out on pithed rabbits with electrically stimulated (2 Hz) sympathetic outflow. Drugs were administered intravenously in a cumulative manner. In conscious rabbits, rilmenidine 0.1, 0.3 and 1.0 mg kg-1 dose-dependently lowered blood pressure, renal sympathetic nerve activity, heart rate and the plasma concentration of noradrenaline and adrenaline. The effect on blood pressure and plasma catecholamines was maximal after 0.3 mg kg-1 whereas heart rate and renal sympathetic nerve activity decreased further after rilmenidine 1.0 mg kg-1. Yohimbine 0.1 and 0.5 mg kg-1, when injected subsequently, attenuated and at the higher dose abolished all effects of rilmenidine. The effects of rilmenidine were also antagonized by the alpha 2-adrenoceptor antagonist 2-(2,3-dihydro-2-methoxy-1,4-benzodioxin-2-yl)-4,5-dihydro-1H-imid azole HCl (RX821002; 0.1 and 0.5 mg kg-1). Yohimbine 0.1 and 0.5 mg kg-1 did not attenuate or attenuated only slightly the decrease of heart rate and renal sympathetic nerve activity produced by infusion of vasopressin. In pithed rabbits with electrically-stimulated sympathetic outflow, yohimbine 0.1 submaximally and yohimbine 0.5 mg kg-1 maximally increased the plasma noradrenaline concentration. The experiments show by direct measurement of sympathetic nerve firing and plasma catecholamines that rilmenidine causes sympathoinhibition in conscious rabbits, presumably through central sites of action.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathoinhibition by rilmenidine in conscious rabbits: involvement of alpha 2-adrenoceptors. 790 76

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