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 short-term effects of ethanol on calcium homeostasis were studied in isolated hepatocytes. Ethanol caused a rapid transient activation of phosphorylase not associated with changes in cAMP levels which peaked after 20-30 s and declined slowly over a period of 5-10 min. Maximal activation was found with 200 mM ethanol, and a significant effect was observed at 25 mM ethanol. Similar effects were induced by other organic solvents and by halothane, with more hydrophobic agents being effective at lower concentrations. In hepatocytes loaded with the intracellular calcium indicator quin2, the addition of ethanol caused a transient increase in cytosolic free calcium, with a kinetic pattern compatible with its involvement in the activation of phosphorylase. Pretreatment of the hepatocytes with phenylephrine or vasopressin to deplete the hormone-sensitive calcium pools in the cells prevented the ethanol-induced calcium mobilization. In 32P-labeled hepatocytes addition of ethanol caused a small (5-7%) decrease in the level of [32P]phosphatidylinositol 4,5-bisphosphate and a 10-15% increase in [32P]phosphatidylinositol 4-phosphate and [32P]phosphatidic acid. In hepatocytes labeled with myo-[3H]inositol, ethanol induced a 50-100% increase in the levels of inositol 1,4,5-trisphosphate, inositol 1,3,4-trisphosphate, and inositol bisphosphate. The changes in the inositol 1,4,5-trisphosphate level due to ethanol paralleled the time course of the elevation of cytosolic free calcium levels and activation of phosphorylase a. The effects of ethanol were comparable to those of a physiologic (1 nM) dose of vasopressin; however, unlike with vasopressin, the inositol phosphates and cytosolic calcium levels declined to basal levels 2 min after the addition of ethanol. These results indicate that ethanol, in common with calcium-mobilizing hormones, activates hormone-sensitive phosphoinositide-specific phospholipase C. The resulting changes in inositol 1,4,5-trisphosphate can account for the mobilization of intracellular calcium and the consequent activation of phosphorylase by ethanol.
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PMID:Ethanol-induced mobilization of calcium by activation of phosphoinositide-specific phospholipase C in intact hepatocytes. 302 63

Effects of dibutyryl-cyclic AMP (db-cAMP) and cyclic AMP (cAMP) microinjected into the hypothalamic supraoptic nucleus (SON) which contains the neurons synthesizing and releasing antidiuretic hormone upon the outflow and the osmotic pressure of urine and the other visceral functions were investigated in water-loaded rats anesthetized with ethanol. When microinjected into the SON the dibutyryl analog of cAMP induced dose-dependent antidiuretic effects without significant effects on any other visceral functions. Dibutyryl-cAMP was much more effective than cAMP; The ED50 value for db-cAMP was approx. 200 nmol versus more than 500 nmol for cAMP. The time course of the antidiuretic effects was relatively slow with minimal urine outflow appearing only after more than 1/2 hour post-injection. The effects induced by db-cAMP demonstrated tachyphylaxis and were partially inhibited by pretreatment with atropine or theophylline, which suggests that the antidiuretic effects were mediated through muscarinic and adenosine receptors present in the nucleus.
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PMID:Antidiuretic effects of dibutyryl-cyclic AMP microinjected into the hypothalamic supraoptic nucleus in water-loaded and ethanol-anesthetized rats. 302 86

Alcohol administration in drinking water to mother rats during gestation resulted in a permanent learning deficit of the offspring when behavioural reactions were tested in active avoidance conditioned reflex situation in adult age. A similar deficit of learning capacity was observed in adult rats following alcohol administration for two weeks; the acquisition of active avoidance response was tested later. Administration of arginine-vasopressin and ACTH 4-10 during behavioural test led to a significant improvement of learning ability of the animals pretreated with alcohol. The observations indicate that the ethanol-induced deficit of learning capacity involves peptidergic mechanisms and the behavioural manifestations following chronic alcohol treatment are not irreversible processes.
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PMID:Effects of arginine-vasopressin and ACTH 4-10 on acquisition of active avoidance response in rats with alcohol pretreatment in prenatal and adult age. 303 47

The effects of ethanol administration on activity and regulation of carnitine palmitoyltransferase I (CPT-I) were studied in hepatocytes isolated from rats fed a liquid, high-fat diet containing 36% of total calories as ethanol or an isocaloric amount of sucrose. Cells were isolated at several time points in the course of a 5-week experimental period. Ethanol consumption markedly decreased CPT-I activity and increased enzyme sensitivity to inhibition by exogenously added malonyl-CoA. Changes in enzyme activity occurred sooner than those in enzyme sensitivity. Fatty acid oxidation to CO2 and ketone bodies was depressed in hepatocytes from ethanol-fed animals during the first part of the treatment. At the end of the 35-day period, there were no longer differences in the rate of ketogenesis between the two groups. At that time, however, the rate of CO2 formation was still impaired in the ethanol-fed animals. Furthermore, addition of ethanol or acetaldehyde to the incubation medium strongly depressed CPT-I activity and rates of fatty acid oxidation in hepatocytes from ethanol-treated rats, whereas these effects were much less pronounced in cells from control animals. The response of CPT-I activity to insulin, glucagon, vasopressin, and phorbol ester was blunted in cells derived from ethanol-fed rats. These changes in the regulation of CPT-I activity corresponded with those observed in the rate of fatty acid oxidation. It is concluded that CPT-I may play a role in the generation of the ethanol-induced fatty liver.
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PMID:Effects of ethanol feeding on the activity and regulation of hepatic carnitine palmitoyltransferase I. 306 12

It has been suggested that vasopressin (VP) and its analogues such as desamino-D-arg8-vasopressin (DDAVP) affect cognitive (including mnemonic) and attentional processes in man. We describe the effects of DDAVP and ethanol (EtOH) on young, healthy human volunteers, using a recently developed visual search task which assesses attention and vigilance. Over a 1-h session, the subject has to detect the occurrence of certain digits in a long list of random characters. A low dose of EtOH (0.33 ml/kg) tended to improve, and a higher dose (1.0 ml/kg) disrupted performance. DDAVP (20 or 60 micrograms/subject) had no effect whatsoever. It is concluded that intranasal administration of the peptide analogue does not markedly affect attention performance in human subjects.
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PMID:Desamino-D-arg8-vasopressin (DDAVP), unlike ethanol, has no effect on a boring visual vigilance task in humans. 309 63

Recent studies have demonstrated the presence of immunoreactive oxytocin (OT) and vasopressin (VP), OT and VP receptors and physiological functions for these two hormones in a variety of peripheral tissues, including anterior pituitary gland. The objectives of this study were to determine if (i) OT and VP genes are expressed in rat testis and anterior pituitary gland and (ii) if osmotic stimulation known to modify the regulation of OT and VP genes in hypothalamus, would modify the expression of these genes in rat testis and anterior pituitary gland. Using oligonucleotide probes (courtesy of Drs. M. Brownstein and W. Scott Young, NIMH) corresponding to the VP gene or OT gene and specific fractions of human OT and VP genes (courtesy of Dr. J. Battey, NCI) subcloned in the pGEM-3 riboprobe system, and Northern blot and slot blot techniques, OT and VP mRNAs were found in rat testis and anterior pituitary gland. When adult male rats (SD) were either deprived of drinking water or offered 2% salt solution as a sole source of drinking fluid for 72 hrs, both OT and VP mRNA levels were increased in hypothalamus, anterior pituitary gland and testis. Our data suggest that testis and anterior pituitary gland could also be sites of synthesis of OT and VP and that the same stimulus may regulate these genes in various tissues.
Adv Alcohol Subst Abuse 1988
PMID:Regulation of vasopressin and oxytocin synthesis in anterior pituitary and peripheral tissues. 322 31

Glucocorticoids inhibit the plasma vasopressin responses to hemorrhage and hypoxia in dogs. Attempts to demonstrate glucocorticoid inhibition of vasopressin secretion in fetal sheep have been unsuccessful, suggesting the possibility that there is an influence of development on the expression of this interaction, or that the interaction cannot be demonstrated in all mammalian species. This study was designed to investigate these two possibilities. Adult ewes chronically prepared with carotid arterial loops, were subjected to 5 hr infusions of cortisol at a rate of 6 ug/kg min or vehicle (5% ethanol in saline). The infusion of cortisol increased plasma cortisol concentration from 26 +/- 3 to 46 +/- 8 ng/ml, while vehicle infusion was associated with a decrease in plasma cortisol concentration from 23 +/- 4 to 15 +/- 3 ng/ml. One hr after the end of the cortisol or vehicle infusions, vasopressin secretion was stimulated by arterial hypotension produced by 10 min infusions of sodium nitroprusside (20 ug/kg min). Nitroprusside decreased arterial blood pressure equally in both groups. Plasma vasopressin concentrations were increased to peak concentrations of 92 +/- 33 and 116 +/- 20 pg/ml in the vehicle- and cortisol-infused groups, responses which were not significantly different as tested by ANOVA. We conclude that increases in plasma cortisol concentration, equal to those observed during responses to stressors, do not inhibit vasopressin secretion in this species.
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PMID:Does cortisol inhibit vasopressin secretion in sheep? 322 18

Five chronic alcoholic patients admitted for detoxification were studied. During the first 24-48 hr of abstinence raised levels of cerebral water (as measured by NMR), vasopressin, renin and supine aldosterone were recorded. Initial vasopressin concentration was correlated (r = 0.88, P less than 0.05) with alcohol consumption in the week prior to admission and was over three times higher in the patients measured after 24-48 hr as compared to less than 24 hr. After one week only supine aldosterone was still raised (P less than 0.05). The results suggest that cerebral oedema occurs during the early stages of abstinence. The role of these changes in the aetiology of withdrawal symptoms, delirium tremens and brain damage remains to be elucidated.
Alcohol Alcohol 1988
PMID:An NMR study of cerebral oedema and its biological correlates during withdrawal from alcohol. 329 84

1. gamma-Aminobutyric acid (GABA) inhibited the antidiuretic response and the increased urinary excretion of vasopressin produced by carbachol when both drugs were injected into a lateral cerebral ventricle (i.c.v.) in the water-loaded rat under ethanol anaesthesia. 2. The inhibitory effect of GABA was mimicked by muscimol and 3-amino-1-propane sulphonic acid (3-APS) and blocked by bicuculline. 3. GABA injected i.v. or into the cisterna magna (i.cist.) did not inhibit the release of vasopressin by carbachol injected i.c.v. 4. The results suggest a role for GABA as a putative inhibitory transmitter in the hypothalamo-neurohypophysial system, acting directly on the supraoptic or paraventricular nuclei in the anterior hypothalamus.
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PMID:Central inhibition by gamma-aminobutyric acid of the release of vasopressin by carbachol in the rat. 335 7

Twenty-seven patients had a first Magnetic Resonance Imaging (MRI) scan 1-3 days after stopping drinking and a second approximately 2 weeks later with no change in whole brain T1 or T1 in selected brain areas. Six patients whose first scan was over 36 h after the last drink underwent an increase in whole brain T1 in the interval to the second scan. The later the first scan was performed the greater was the increase in T1. These results are compatible with a very early fall in brain water immediately on cessation of drinking (perhaps due to a rebound increase of vasopressin activity) with a return to 'baseline' after two weeks. A third scan after discharge from hospital in 23 individuals who had abstained from alcohol or drank very little did not reveal any further significant change in brain T1.
Drug Alcohol Depend 1988 Feb
PMID:Brain hydration during alcohol withdrawal in alcoholics measured by magnetic resonance imaging. 336 51


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