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)

1. Vasopressin (anti-diuretic hormone, [8-arginine]vasopressin) inhibited the synthesis de novo of fatty acids (measured with (3)H(2)O and U-(14)C-labelled lactate or U-(14)C-labelled glucose) and stimulated glycogen breakdown in the perfused liver of fed mice. 2. The concentration dependence of these effects (range 200-1000muunits/ml, i.e. 0.5-2.5ng/ml) resembled that for the action on glycogen breakdown which was previously reported for rat liver. 3. The appearance of newly synthesized fatty acids in both phospholipids and triglycerides was inhibited by vasopressin, whereas synthesis of cholesterol was less affected. 4. Inhibition of hepatic lipogenesis by vasopressin is the most potent short-term hormonal action on this process yet reported. Aspects of the effect are discussed, including the lack of a role for cyclic AMP, and a possible link with vasopressin action on glycogen metabolism.
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PMID:Inhibition of fatty acid synthesis and stimulation of glycogen breakdown by vasopressin in the perfused mouse liver. 122 Jun 92

The intracarotid infusion of hypertonic sodium chloride in anesthetized dogs pretreated with vasopressin and mineralocorticoid resulted in an increase in sodium excretion as well as an increase in the percent of the filtered load of sodium excreted. This increase was not due to changes in renal hemodynamics or arterial blood pressure. The change in fractional sodium excretion was approximately 1%. Intracarotid infusion of isotonic sodium chloride did not result in a natriuretic response. The intracarotid infusion of hyperosmotic glucose did not evoke an increase in sodium excretion. Femoral vein infusions of hypertonic sodium chloride failed to evoke any natriuretic response. These data indicate that a sodium-sensing mechanism may exist in the brain that can alter the renal handling of sodium. The efferent mechanism of the response is discussed.
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PMID:Natriuresis induced by intracarotid infusion of hypertonic NaCl. 125 24

The effects of iso-osmolar and hypo-osmolar volume expansion on renal water and sodium excretion were studied in dogs during light chloralose anesthesia. Saline or a hypo-osmolar of glucose and urea was given i.v. (20 ml/kg b.w.t. in 60 min). From the start of this infusion the combined weight of the hydration infusate and the dog was maintained constant by a servo system, which controlled the rate of infusion of a hypo-osmolar solution. Consequently the degree of hydration increased linearly during the infusion period after which it remained constant throughout the experiment. No increase in free water clearance was seen after iso-osmolar volume expansion. The rate of excretion of sodium increased considerably. Hypo-osmolar volume expansion provoked a water diuresis during which the rate of excretion of sodium fell to less than 0.1 mumol/kg b.w.t. min. It is concluded that under the present circumstances infusion of iso-osmolar saline is not associated with a decrease in the rate of secretion of vasopressin.
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PMID:Effects on renal water and sodium excretion of infusions of either iso-osmolar saline or a hypo-osmolar solution of non-electrolytes. 127 14

Brain death is associated with loss of hypothalamic, pituitary and brain stem function resulting in apnea, bradycardia and hypotension, poikilothermia, and diabetes insipidus. In order to preserve body functions mechanical ventilation is continued with the aim to maintain an arterial partial pressure of oxygen of more than 100 mmHg. Previous fluid restrictions and the application of diuretics during the treatment of high intracranial pressure frequently result in dehydration. Progressive vasodilation may induce severe hypotension and fluid replacement with cristalloids and if necessary colloids may be called for until the central venous pressure reaches 10 cm H2O. Continuous substitution of potassium and the use of hypotonic solutions such as glucose 5% may avoid hypokalaemia and hypernatraemia, respectively. Inotropic support with dopamine (5-10 micrograms/kg.min) or adrenaline (0.01-0.1 micrograms/kg.min) may be needed to maintain normal mean arterial blood pressure (65 mmHg). Polyuria (5000 ml/24 h) can be treated by continuous intravenous infusion of antidiuretic hormone (0.5-2-10 U/h). Hypothermia must be prevented by warming all fluids (37 degrees C) and covering the patient with heat saving blankets.
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PMID:[Management of the organ donor]. 128 68

A 77-year-old man developed syncope after meals at the age of 75. He had been treated with anti-Parkinson's drugs such as levodopa for 18 years as a patient with idiopathic Parkinson's disease (PD). The medications had been very effective to his parkinsonism. Ambulatory blood pressure was recorded every 20 minutes throughout one day by indirect measurement using a Colin medical instrument monitor (ABPM-630). The subsequent data disclosed that postprandial hypotension (PPH) was associated with the frequent after-meal syncope. It was also found that oral ingestion of a solution containing 50 grams of glucose caused a marked and prolonged hypotension during the resting supine position. Plasma norepinephrine failed to show any increment. Plasma vasopressin slightly increased while pulse rate, plasma renin activity, osmolality, and hematocrit did not change despite the production of severe hypotension of a relative acute onset. Signs of glucose intolerance and hyperinsulinemic response were observed. Indications of systemic autonomic nervous dysfunctions were revealed in various autonomic nervous function tests. Physical treatment combined with medication such as droxidopa, midodrine and especially caffeine and fludrocortisone proved to be effective on PPH. The authors confirmed the existence of PD with symptomatic PPH. In addition, we considered this present case as an example of "progressive autonomic failure with PD" (Bannister, 1988).
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PMID:[Parkinson's disease with syncope as a chief complaint induced by prominent postprandial hypotension]. 130 Feb 58

This study has examined the effects of insulin-induced hypoglycemia on expression of the CRH, arginine vasopressin, and POMC genes and corresponding peptides in freely moving, unanesthetized, male Sprague-Dawley rats. Animals were infused with 150 mM NaCl for 3 days before the experimental day and were then administered insulin (4 U/kg) or saline iv. In one experiment animals were killed 0, 30, 60, or 90 min after insulin or saline, and RNA was isolated from anterior pituitary, cerebral cortex, and punches of the hypothalamic paraventricular and supraoptic nuclei. In a second experiment, animals were killed 90 min after insulin or saline treatment, and RNA was isolated from whole hypothalami. RNA was analyzed by Northern blot. Plasma glucose fell from 106 +/- 5 to 38 +/- 2 mg/dl after insulin administration and remained low for the duration of the experiment. Plasma levels of ACTH, corticosterone, and vasopressin were 10-, 6-, and 4-fold higher, respectively, in the insulin-treated vs. control animals (by analysis of variance, P less than 0.0001 in all cases), while plasma CRH was unchanged. During hypoglycemia POMC mRNA levels were 1.8-fold higher in the insulin-treated group (by analysis of variance, P less than 0.025). In contrast, paraventricular nucleus, whole hypothalamic, and parietal cortex CRH mRNA and vasopressin mRNA were unchanged. These data support previous studies which indicated that POMC gene expression is increased by hypoglycemia. However, we found no evidence for an increase in paraventricular nucleus or cerebral cortex CRH mRNA expression during hypoglycemia-associated stimulation of the hypothalamic-pituitary-adrenal axis, suggesting that another factor(s) may mediate the observed increase in POMC gene expression.
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PMID:The effect of insulin-induced hypoglycemia on gene expression in the hypothalamic-pituitary-adrenal axis of the rat. 131 Feb 84

We evaluated whether the brain kallikrein-kinin system plays a role in the regulation of adrenocorticotropin (ACTH) release in rats. Intracerebroventricular (icv) injection of bradykinin (0.24 nmol) increased plasma immunoreactive ACTH (irACTH) levels (from 93 +/- 4 to 200 +/- 12 pg/ml, P less than 0.01). This effect was prevented by icv kinin antagonist at 15.4 nmol/h (from 98 +/- 5 to 108 +/- 6 pg/ml; not significant). The antagonist did not alter the increase in plasma irACTH levels induced by icv corticotropin-releasing factor (CRF), arginine vasopressin, or prostaglandin E2. Melittin (7 nmol/h icv) increased plasma irACTH from 95 +/- 4 to 268 +/- 7 pg/ml (P less than 0.01). This effect was prevented by icv kinin antagonist (15.4 nmol/h), kallikrein antibodies (13 pmol/h), or indomethacin (0.28 mmol/h). ACTH response to melittin was not altered by antagonists of CRF or vasopressin. Intra-arterial injection of insulin (0.3 IU/kg body wt) reduced plasma glucose levels to a similar extent in rats given icv kinin antagonist or vehicle; the ACTH response to insulin-induced hypoglycemia was slightly less in rats given kinin antagonist than in those given vehicle (55 +/- 5 vs. 86 +/- 4 pg/ml, P less than 0.05). The brain kallikrein-kinin system may play a role in the regulation of ACTH secretion in stimulated conditions.
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PMID:Role of brain kallikrein-kinin system in regulation of adrenocorticotropin release. 131 88

Fructose-1,6-diphosphate (FDP) is a physiological product which exhibits pharmacological properties. This study shows that FDP (1-3 mM) inhibits platelet aggregation induced by the agonists thrombin, vasopressin, platelet activating factor, ADP, adrenaline, arachidonate and the stable thromboxane analogue U 44069. Thrombin-promoted ATP secretion and cytosolic Ca2+ rise are also drastically inhibited by FDP, which decreases, although to a lesser extent, the protein kinase C-dependent phosphorylation of the 47 kDa protein. The inhibition on thrombin-induced aggregation is shared, albeit less efficiently, by glucose-1,6-diphosphate and fructose-2,6-diphosphate but not by other phosphorylated monosaccharides (fructose-1:2 cyclic,6-diphosphate, glucose-1- and glucose-6-phosphate, fructose-1- and fructose-6-phosphate, mannose-6-phosphate and 5-phosphoryl ribose-1-pyrophosphate). FDP does not affect platelet activation induced by the protein kinase C activators dioctanoylglycerol or phorbol 12-myristate 13-acetate. No increase of cAMP concentration is observed in FDP-treated platelets. Altogether, these results indicate that FDP inhibits platelet activation at a level preceding phospholipase C. The data are consistent with a general inhibitory action of FDP on signal transmission.
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PMID:Fructose-1,6-diphosphate inhibits platelet activation. 131 5

To elucidate the acute effect of insulin on its receptor, rat adipocytes were preincubated with insulin, washed with KCN to inhibit receptor cycling, and 125I-labeled insulin binding was measured. Preincubating cells from young insulin-sensitive rats with insulin increased cell surface binding up to approximately fourfold without changing apparent receptor affinity. This effect was rapid (t1/2 less than 5 min) and had a similar dose-response relationship as the effect on glucose transport. It was also energy dependent because preincubation with KCN completely abolished the effect of subsequent insulin exposure. The increased binding capacity was not recovered after cell solubilization or in partially purified receptors or isolated plasma membranes. Cells pretreated with insulin were less sensitive to the ability of trypsin to remove cell surface receptors, suggesting a conformational change of the receptors. This was also supported by the finding that the polyclonal binding in insulin-treated but not in control cells. Vanadate mimicked the effect of insulin to increase insulin binding, whereas concanavalin A, vasopressin, phorbol esters, or the adenosine analogue phenyl isopropyl adenosine was without effect. Insulin-resistant adipocytes from obese rats displayed no increase in cell surface binding after insulin treatment, despite normal tyrosine kinase activity in response to insulin. Thus, both insulin and vanadate elicit a rapid effect to markedly increase the number of cell surface insulin binding sites in intact rat adipocytes. This appears to occur independently of protein kinase C and the inhibitory GTP binding protein (Gi). Furthermore, the effect of insulin could not be demonstrated in insulin-resistant cells, suggesting that this mechanism may be of importance for the regulation of insulin sensitivity.
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PMID:Insulin can rapidly increase cell surface insulin binding capacity in rat adipocytes. A novel mechanism related to insulin sensitivity. 131 56

Various polypeptide hormones including vasopressin (VP) and gastrin-releasing peptide (GRP) are produced by small cell lung carcinomas (SCLC). VP as well as GRP have mitogenic effects on several cell types and are proposed to be autocrine growth factors. In this study the presence of VP mRNA, oxytocin (OT) mRNA and GRP mRNA was investigated in cell lines derived from SCLCs. Out of 26 cell lines 3 contained low amounts of VP mRNA (GLC-8, SCLC-21H and NCI-H345) and 7 contained abundant GRP mRNA (GLC-16, GLC-1-M13, SCLC-22H, NCI-H249, NCI-H345, NCI-H449 and NCI-H450). The GRP mRNA-containing cell lines belong to the classic SCLC type, whereas VP mRNA was found in two classic and one variant cell line. None of the SCLC cell lines contained detectable levels of OT mRNA. Of the three VP-expressing SCLC cell lines, GLC-8 had the highest level of VP mRNA. Both the length of the transcript and the hybridization with different probes containing exons A and C of the VP gene suggest that the detected transcript is a normal VP messenger. SCLC GLC-8 contained low levels of VP immunoreactivity and VP receptors. In GLC-8 an autocrine role of VP may be suspected.
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PMID:Expression of the vasopressin and gastrin-releasing peptide genes in small cell lung carcinoma cell lines. 132 Aug 93


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