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)

Rats given ethanol in their drinking water at a concentration that permitted adequate fluid intake gradually accepted higher concentrations and consumed larger amounts of ethanol. These increases were augmented when daily subcutaneous injections of 1 microgram of desglycinamide9-lysine8-vasopressin (DGLVP) or 10 microgram of prolyl-leucyl-glycinamide (PLG) were given concomitantly. Nonsignificant changes in ethanol consumption were seen with injections of 1 microgram PLG, or 0.42 or 42 microgram of lysine8-vasopressin (LVP). In a second experiment 4 microgram DGLVP given every second day as a long-acting zinc phosphate complex, commencing after the increases in ethanol intake had taken place, failed to produce any change in ethanol consumption subsequently. In both Experiments 1 and 2, the rats were switched from forced ethanol intake to a choice between ethanol and tap water. On these tests there was only marginal evidence of peptide-produced changes in ethanol intake.
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PMID:Effect of desglycinamide(9)-lysine(8)-vasopressin and prolyl-leucyl-glycinamide on oral ethanol intake in the rat. 3 34

Ethanol (9%) decreases the potential difference across the toad bladder when present at the mucosal surface, the short-circuit current was unchanged. The electrical resistance decreased indicating a change in ion movements across the bladder. Unidirectional 22Na and 36Cl flux measurements showed an increase in the movement of Cl, but no change in Na. The vasopressin-induced increase in Na transport (natriferic response) was also unaffected by the presence of ethanol. It is suggested that ethanol may be altering the apical tight junctions and affecting an anion selective pathway. The hydro-osmotic response of the toad bladder to vasopressin was decreased by 70% in the presence of 3% ethanol. The hydro-osmotic action of cyclic adenosine monophosphate was also inhibited by ethanol, indicating an action subsequent to the endogenous formation of this nucleotide. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. The vasopressin-induced increase in diffusional water flow was similarly reduced. Osmotic water movements across glutaraldehyde and N-ethylmaleimide-"fixed" vasopressin-stimulated bladders were also decreased in the presence of ethanol. However, 3% ethanol had no effect on osmotic water transfer across artificial collodion membranes. Ethanol, therefore, probably interacts with the bladder membrane. The Ktrans (permeability coefficient) of ethanol and water is increased by vasopressin. suggesting that their movement is through similar pathways. It is suggested that ethanol empedes the flow of water across the toad bladder by facilitating a physicochemical interaction between the membrane "pore" and the water molecules.
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PMID:Effects of ethanol on the permeability of toad urinary bladder epithelium. 5 35

The histochemical, immunohistological and histoenzymatic study of the hypothalamo-neurohypophysial system of the rat shows that chronic ethanol administration induces: a temporary blockage of vasopressin synthesis, a vasoconstriction of the neurohypophysial capillaries, a dendritic storage of immunoreactive vasopressin. In our experimental conditions, a long ethanol treatment disturbs the balance between vasopressin synthesis and release.
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PMID:[Changes in rat hypothalamo-neurohypophyseal system after repeated ethanol administration]. 12 25

The effects of ethanol on the water permeability and short-circuit current of the isolated urinary bladder of the toad, Bufo marinus, were investigated. Ethanol alone did not alter the flow of water along an osmotic gradient. The increase in osmotic water flow caused by vasopressin, theophylline or cyclic adenosine-3',5'-monophosphate was inhibited by 4 to 40 mg per ml of ethanol in the mucosal or serosal bathing medium. The inhibition was more marked when ethanol was added to the serosal bathing medium, in spite of the increase in the osmotic gradient across the toad bladder caused by the ethanol. Ethanol had no effect on the increase in sodium transport (short-circuit current) due to vasopressin, although there was a significant inhibition of base-line short-circuit current. It is possible that the water diuresis due to ethanol may result in part from an inhibition of the effect of vasopressin on the collecting duct.
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PMID:Effect of ethanol on the water permeability and short-circuit current of the urinary bladder of the toad and the response to vasopressin, adenosine-3',5'-monophosphate and theophylline. 17 29

Urinary excretion of adenosine 3',5' -cyclic monophosphate (cAMP) and immunoreactive arginine vasopressin (AVP) were investigated after water loading and following ethanol loading in two rat strains selected for their voluntary ethanol intake. After ethanol loading ethanol preferring (AA) rats excreted more cAMP but less AVP than water preferring (ANA) rats. The results suggest that the strain difference in cAMP excretion is of renal origin and is not due to vasopressin or parathormone. Differences in the sympathetic nervous activity may be responsible for the difference in cAMP excretion.
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PMID:Urinary cyclic AMP and vasopressin excretion in rat strains selected for their alcohol intake. 20 97

The role of pituitary vasopressin (antidiuretic hormone--ADH) in the formation and dynamics of aqueous humour was studied in rabbits employing different techniques. Using isolated ciliary body preparations the changes in transepithelial short-circuit current were measured, and natural vasopressin and Lys8-vasopressin were found to increase the transepithelial short-circuit current at concentrations less than 10 muU/ml (i.e. within the physiological range), indicating increased sodium transport across the ciliary epithelium. In another series of experiments with intact rabbits given an ethanol load to suppress endogenous ADH, administration of exogenous vasopressin raised the intraocular pressure, and a similar effect was observed when endogenous ADH production was stimulated with nicotine. Direct measurements of outflow showed that vasopressin was without effect when given intravenously and that the only effect when given intracamerally was to increase the facility which would tend to lower rather than raise the intraocular pressure. Finally, the intra-arterial and intravenous effects of vasopressin on circulation in the iris and on the intraocular and systemic arterial pressures were studied. Local effects on the vascular bed in the eye and changes in systemic blood pressure were observed only at rates of administration well in excess of the physiological range for endogenous vasopressin production. It is concluded that, at physiological levels, antidiuretic hormone can stimulate active sodium transport into the eye thereby tending to raise the intraocular pressure, and it is suggested that this may act as a homeostatic regulating mechanism limiting changes in the rate of formation of aqueous humour and in intraocular pressure which might otherwise result from diurnal variations in the state of body hydration. This also offers some explanation for the ocular hypotensive action of ethanol.
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PMID:Role of pituitary vasopressin in the formation and dynamics of aqueous humour. 28 4

Ethanol and drugs can affect each other's absorption, distribution, metabolism, and excretion. When ingested together, ethanol can increase drug absorption by enhancing the gastric solubility of drugs and by increasing gastrointestinal blood flow. However, high concentrations of ethanol induce gastric irritation causing a pyloric spasm which in turn may delay drug absorption and/or reduce bioavailability. The 'quality' of the alcoholic beverage, independent of its ethanol content, can contribute to altered absorption of a drug. Ethanol is not bound to plasma proteins extensively enough to modify drug distribution. However, serum albumin levels in chronic alcoholics may be abnormally low so that some drugs, e.g. diazepam, have an increased volume of distribution. In addition to the amount ingested, the duration of regular intake determines the effect of ethanol on drug metabolism. Acute intake of ethanol inhibits the metabolism of many drugs but long term intake of ethanol at a high level (greater than 200g of pure ethanol per day) can induce liver enzymes to metabolise drugs more efficiently. At the present time there are no accurate means, with the possible exception of liver biopsy, to clinically predict the capacity of an alcoholic to metabolise drugs. Several drugs can inhibit the metabolism of ethanol at the level of alcohol dehydrogenase. Individual predisposition determines the severity of this drug-ethanol interaction. During its absorption phase, ethanol inhibits the secretion of antidiuretic hormone and is also able to induce increased excretion of a drug through the kidneys. However, chronic alcoholics with water retention may show reduced excretion of drugs via this route. At the pharmacodynamic level, ethanol can enhance the deleterious effects of sedatives, certain anxiolytics, sedative antidepressants and antipsychotics and anticholinergic agents, on performance. Mechanisms of lethal interactions between moderate overdoses of ethanol and anxiolytics/opiates/sedatives are poorly understood. On the other hand, certain peptides, 'nonspecific' stimulants, dopaminergic agents and opiate antagonists can antagonise alcohol-induced inebriation to a significant degree.
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PMID:Drug interactions with alcohol. 38 74

Ethanol, like other anesthetics, has been reported to interfere with active Na+ transport in living membranes. In an attempt to elucidate the mechanism by which ethanol exerts this action, we tested in the toad bladder membrane: 1) the effect of ethanol on active Na+ transport, 2) the interaction of ethanol with vasopressin on Na+ transport, and 3) the effect of ethanol on passive Na+ flux. We found that, a) 1-500 microgram/ml of ethanol stimulated, and 10,000 microgram/ml depressed active Na+ transport; b) the combined effect of stimulating concentrations of ethanol and vasopressin, although suggestive of a positive interaction, might have arisen by chance (p = 0.08); c) depressant concentrations of ethanol failed to suppress the stimulation by vasopressin; and d) passive Na+ flux in bladders treated with ouabain and ethacrynic acid was not affected by ethanol (1-100 microgram/ml). These results indicate that ethanol in concentrations ranging from 1 to 10,000 microgram/ml does not block ATP/ATPase Na+ pump but apparently exerts a dose-dependent, stimulant-depressant effect on Na+ channels in the membrane.
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PMID:Ethanol effects on active and passive Na+ flux in toad bladder. 41 65

The concentration of blood vasopressin was investigated in apparently healthy persons and in patients with I--II degree hypertension, aged from 20 to 80 years. Vasopressin concentration was determined by the biological method according to the antidiuretic effect of ethanol-anesthetized and constantly hydrated rats on an original 5-channel apparatus. The results obtained showed the blood vasopressin concentration to increase with age. In patients with the I--II degree hypertensive disease the mentioned concentration was significantly higher than in healthy persons of the same age. Close correlation coefficient was revealed between the blood vasopressin concentration and minimal arterial blood pressure values.
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PMID:[Blood vasopressin concentration is patients of different ages with hypertension]. 47 71

A simple efficient procedure for extracting and concentrating arginine-8-vasopressin (AVP) from urine has been coupled with a specific and sensitive radioimmunoassay in order to measure antidiuretic hormone (ADH) excretion in normal humans under various physiological stimuli. Antisera have been raised in rabbits injected with lysine-vasopressin (LVP) or AVP coupled with bovine serum albumin. The antiserum selected for the assay which inhibits the antidiuresis induced in the rat by AVP is used at a final dilution of 1 : 50,000 and possesses a high association constant of 1 x 10(11) 1.mol-1. The limit of detection of the RIA system is 0.5 micronUI/ml of urine (1.25 pg). Urinary ADH has been extracted from urine by Miller and Moses method. Mean recovery of added vasopressin averaged 90.2% +/- 11 (SD) and assay of serial dilutions of such extracts showed that they behave in the assay system in the same way as synthetic AVP standards. Moreover comparison of the results obtained by the RIA to those given by the biological method using the ethanol anesthetized rat showed excellent correlation (r = 0.9 p less than 0.001). Under ad libitum fluid and food intake, mean daily urinary excretion of AVP (uncorrected for recovery) determined in 22 subjects was found to be 30.58 +/- 11.64 mU/h with no significant difference between men and women. In response to an oral waterload ADH became undetectable at the peak of diuresis. Following a 16 hr fluid deprivation, ADH rose moderately. A significant correlation has been found between urine osmolality and AVP excretion rate.
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PMID:[Radioimmunoassay of ADH in human urine (author's transl)]. 47 16


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