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)

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 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

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

Ethanol (3%) decreases the potential difference and short-circuit current across the isolated frog skin in chloride Ringer's solution. Unidirectional fluxes of Na and Cl indicate that the drop in short-circuit current is due to an inhibition of the sodium influx. However, ethanol had no effect on the electrical parameters or sodium fluxes, when the frog skin was bathed in chloride-free solutions on both sides or the outside alone. The ethanol response is anion-dependent. In addition, chloride-free media in the inside bathing solution reduced the short-circuit current, indicating a sodium transport pathway which is dependent on chloride and confirming previous data in the literature. Other anions such as sulfate and nitrate could not substitute for chloride. The vasopressin-induced natriferic response and the ethanol effect were found to work independently of each other and different pathways of action are suggested for these agents. The intracellular sodium content of the isolated frog skin epithelium increased and potassium decreased in the presence of the Na-K adenosine triphosphatase inhibitor, ouabain, whereas ethanol or amiloride had no effect. The oxygen consumption of the isolated frog skin was unaffected by up to 10% ethanol. A general metabolic action is probably thus not mediating the response. Urea, in iso-osmotic concentrations to the ethanol, did not mimic its effect. Tritiated water fluxes (in the absence of an osmotic gradient) were reduced by 30% in the presence of 3% ethanol. It is suggested that ethanol may impede the flow of water across frog skin by a physicochemical interaction with membrane pores and the water molecules. The permeability coefficient (Ktrans) for ethanol was found to be 10 times smaller than the Ktrans for water.
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PMID:Effects of ethanol on the permeability of frog skin. 108 5

We have investigated the feasibility of monitoring local skeletal muscle blood flow in the rat by including ethanol in the perfusion medium passing through a microdialysis probe placed in muscle tissue. Ethanol at 5, 55, or 1100 mM did not directly influence local muscle metabolism, as measured by dialysate glucose, lactate, and glycerol concentrations. The clearance of ethanol from the perfusion medium can be described by the outflow/inflow ratio ([ethanol]collected dialysate/[ethanol]infused perfusion medium), which was found to be similar (between 0.36 and 0.38) at all ethanol perfusion concentrations studied. With probes inserted in a flow-chamber, this ratio changed in a flow-dependent way in the external flow range of 5-20 microliters min-1. The ethanol outflow/inflow ratio in vivo was significantly (P less than 0.001) increased (to a maximum of 127 +/- 2.8% and 144 +/- 7.4% of the baseline, mean +/- SEM) when blood flow was reduced by either leg constriction or local vasopressin administration, and significantly (P less than 0.001) reduced (to 62 +/- 6.4% and 43 +/- 4.4% of baseline) with increases in blood flow during external heating or local 2-chloroadenosine administration, respectively. Dialysate glucose concentrations correlated negatively with the ethanol outflow/inflow ratio (P less than 0.01) and consequently decreased (to 46 +/- 7.6% and 56 +/- 5.6% of baseline) with constriction and vasopressin administration and increased (to 169 +/- 32.5% and 262 +/- 16.7% of baseline) following heating and 2-chloroadenosine administration. Dialysate lactate concentrations were significantly increased (approximately 2-fold, P less than 0.001) during all perturbations of blood flow. In conclusion, this technique makes it possible to monitor changes in skeletal muscle blood flow; however, methods of quantification remain to be established. The fact that blood flow changes were found to significantly affect interstitial glucose and lactate concentrations as revealed by microdialysis indicates that this information is critical in microdialysis experiments.
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PMID:The ethanol technique of monitoring local blood flow changes in rat skeletal muscle: implications for microdialysis. 144 30

Anterior pituitary corticotrope function was analyzed in the long sleep (LS) and short sleep (SS) lines of mice selectively bred for differences in sensitivity to ethanol. In vivo challenge with acute ethanol or CRH administration or the stress of novel handling resulted in a more pronounced increase in serum corticosterone levels in LS mice compared with SS mice. Likewise, in vivo administration of ethanol resulted in 3-fold higher levels of anterior pituitary pro-ACTH/endorphin mRNA in LS mice compared with SS mice. However, this differential regulation of the HPA axis during in vivo analysis was not observed during in vitro studies of anterior pituitary corticotrope function. Primary cultures of LS and SS anterior pituicytes responded appropriately but equivalently to a variety of secretagogues known to stimulate anterior pituitary ACTH secretion. These secretagogues included CRH (10 nM), dibutyryl-cAMP (1 mM), vasopressin (100 nM), and phorbol 12-myristate 13-acetate (10 nM). Ethanol had no direct stimulatory effect on pituitary ACTH secretion. Quantitation of anterior pituitary corticotrope peptide biosynthesis was determined by immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis of extracts from [35S]methionine-labeled anterior pituitary explants and from [35S]methionine-labeled primary cultures of anterior pituitary cells. LS mice pro-ACTH/endorphin biosynthesis in pituitary explants was 2-fold greater than pro-ACTH/endorphin biosynthesis in SS mice pituitary explants. However, in culture, isolated from hypothalamic and adrenal factors, the LS anterior pituitary pro-ACTH/endorphin biosynthetic rate became equivalent to the SS anterior pituitary pro-ACTH/endorphin biosynthetic rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential regulation of anterior pituitary corticotrope function is observed in vivo but not in vitro in two lines of ethanol-sensitive mice. 168 69

Addition of ethanol (17 to 340 mM) to cultured rat hepatocytes stimulated the breakdown of phosphatidylcholine phospholipases D and C as measured by an increase in the rate of release of choline and phosphocholine into the medium. The effects of ethanol were mimicked by propanol, dimethylsulfoxide and to a lesser extent methanol. The magnitude of the stimulation seen with ethanol was equivalent to and additive to that produced by glucagon vasopressin, norepinephrine, A23187 or PMA. In contrast, ethanol (340 mM) stimulated PI-specific phospholipase C activity by less than 20%. An equivalent stimulation of PC-specific phospholipase D and C was seen with as little as 20 mM ethanol and a 100% increase was seen with 340 mM ethanol. Ethanol did not significantly affect the ability of vasopressin, norepinephrine, ATP or A23187 to stimulate PI-specific phospholipase C. It is concluded that while ethanol is only a weak stimulator of PI-specific phospholipase C, it is a potent stimulator of phosphatidylcholine breakdown in rat hepatocytes.
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PMID:Ethanol is a potent stimulator of phosphatidylcholine breakdown in cultured rat hepatocytes. 173 64

The effect of ethanol on receptor-mediated phospholipase C-linked signal transduction processes was investigated in isolated rat hepatocytes. Pretreatment of the cells with ethanol (6-300 mM) markedly inhibited a subsequent stimulation of phospholipase C by vasopressin, angiotensin II, or epidermal growth factor. By contrast, the effects of the alpha 1-adrenergic agonist phenylephrine and of glucagon were not affected by ethanol pretreatment. Ethanol inhibited the agonist-induced decrease in polyphosphoinositides, the formation of inositol phosphates, and the increase in cytosolic free Ca2+ levels, as detected with the intracellular Ca2+ indicator indo-1. The effects of ethanol were concentration dependent and were pronounced at low concentrations of agonists but were not significant at saturating levels. Pretreatment of the cells with the protein kinase C inhibitor H7 partly prevented the inhibition by ethanol of vasopressin-induced phospholipase C activation. By contrast, pretreatment of the cells with (Rp)-adenosine cyclic 3':5'-phosphorothioate [Rp)-cAMP-S), a competitive inhibitor of protein kinase A, potentiated the inhibitory effect of ethanol on the Ca2+ mobilization by vasopressin. (Rp)-cAMP-S similarly potentiated the inhibition of phospholipase C by the protein kinase C-activating phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA). The kinase A inhibitor also made the Ca2+ mobilization by phenylephrine sensitive to ethanol, indicating that the formation of cAMP in the cells played a role in suppressing the sensitivity to ethanol. Pretreatment of the cells with ethanol enhanced the inhibitory effects of TPA on the vasopressin-induced phospholipase C activation at all concentrations of the hormone; however, these synergistic effects were prevented when TPA was added prior to ethanol, a condition that prevents the activation of phospholipase C by ethanol. The data indicate that ethanol causes desensitization of the receptor-mediated phospholipase C secondary to the ethanol-induced activation of phospholipase C and activation of protein kinase C. Ethanol treatment also affects the sensitivity of the phospholipase C system to control by protein kinases A and C. The data indicate that ethanol can affect the control of intracellular signal transduction processes in liver cells under physiologically relevant conditions.
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PMID:Ethanol causes desensitization of receptor-mediated phospholipase C activation in isolated hepatocytes. 184 16

The role of vasopressin in the development of gastric hemorrhagic erosions induced by the oral administration of 1 mL of 75% ethanol in rats was studied. The area of the lesions in homozygous Brattleboro rats, having a defective vasopressin synthesis, was only 20% of that found in Wistar and heterozygous Brattleboro rats, which have normal vasopressin production. It is well known that vasopressin acts via the V1 (pressor) and V2 (antidiuretic) receptors. Administration of V1 and V2 vasopressin-receptor agonists and antagonists in this model showed that pressor-receptor activity is needed for the generation of all lesions in Wistar and heterozygous Brattleboro rats. Ethanol damage to the gastric mucosa was diminished by the V1 antagonist with similar efficacy as in the case of a vasopressin deficiency. Administration of the V1 antagonist and the absence of endogenous vasopressin were shown to protect the deeper layer of the gastric mucosa (assessed by histology) and to reduce significantly the ethanol-induced vascular injury and increase in vascular permeability (assessed by the monastral blue technique). Thus, endogenous vasopressin is clearly of great importance in the pathogenesis of gastric hemorrhagic lesions induced by ethanol. These results strongly suggest that vasopressin is an endogenous aggressor toward the gastric mucosa.
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PMID:The role of vasopressin in the pathogenesis of ethanol-induced gastric hemorrhagic erosions in rats. Is vasopressin an endogenous aggressor toward the gastric mucosa? 193 94


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