Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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)
Alcohol Clin Exp Res 1990 Feb
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

We studied the effect of ethanol on the phosphorylation of cytokeratins (CKs) in cultured hepatocytes since CK filaments are regulated by phosphorylation and they are abnormal in alcoholic liver disease. Hepatocytes were obtained from 14-day-old rats and cultured for 48 hrs. The hepatocytes were exposed to ethanol (300 mM) for 30 min. The cells were extracted with the buffer containing Triton X-100. The residual insoluble cytoskeletons were analyzed by two dimensional (2D) gel electrophoresis and autoradiography. 2D gel electrophoresis showed CK 55 and CK 49 or 8 and 18 and actin. The CKs had several isoelectric variants. The most basic spot was the dominant protein which was not phosphorylated. The more acidic spots were phosphorylated. After ethanol treatment, the phosphorylation of CK 55 and CK 49 were markedly increased over controls. We compared these results, with the effect of vasopressin (10 nM), TPA (150 nM) and db-cAMP (1 mM) on the phosphorylation of CKs. Vasopressin and TPA caused the phosphorylation of CK 55 and 49 but db-cAMP did not. The results suggest that CKs are phosphorylated by protein kinase C through the phosphoinositide-linked transduction system activated by ethanol.
 ...
PMID:Ethanol-induced phosphorylation of cytokeratin in cultured hepatocytes. 169 3

Ten male patients scheduled for transurethral prostatic resection (aged 57-79) were given irrigating fluid by intravenous infusion at 50 ml.min-1 over 20 min. Each patient was subjected to two infusions: 1.5% glycine in water on one occasion, and the same solution but with 1% ethanol added on the other. Urine and blood samples were collected at regular intervals for up to 2 h after infusion, and the changes in the distribution of water and electrolytes between fluid compartments were calculated. Transient prickling skin sensations were frequently reported effects of the infusions. Two patients experienced visual disturbances. There were no changes in the blood ammonia and plasma vasopressin levels. During the infusions, the estimated blood volume and the total plasma sodium and potassium content increased. The solutions produced osmotic diuresis with increased urinary excretion of water and electrolytes. After ending the fluid administration, blood volume was rapidly restored. Over the following 120 min the irrigant water was redistributed intracellularly or removed by urinary excretion. The addition of ethanol did not alter the overall effects of glycine solution on the fluid balance.
 ...
PMID:Effects of 1.5% glycine solution with and without 1% ethanol on the fluid balance in elderly men. 172 75

As vasopressin (VP) has been related to tolerance, we were interested in following central VP levels after chronic alcohol exposure of two selected mouse lines (C57Bl and Balb/c). Strongly elevated VP and VP mRNA levels have been noted, in particular in the hypothalamus. The phenomenon is much more marked in Balb/c mice than in C57Bl; in extrahypothalamic areas in the changes in VP noted in septum and amygdala are only apparent in Balb/c mice. Hypothalamic norepinephrine and serotonin, known to partly control VP release, also reacts in a strain dependent manner to alcohol. This study provides neurochemical evidence that long term ethanol intoxication selectively activates central vasopressinergic and aminergic neurons in mice. Such activation appears to be strain dependent; therefore it may be related to the unequal capacities of these strains to adapt to chronic alcohol intoxication. Such phenomena may partly account for differences between individuals in tolerance to chronic alcohol in men.
Alcohol Alcohol Suppl 1991
PMID:Are chronic alcohol-induced central vasopressin changes determinant in strain dependency of tolerance in mice? 172 85

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.
 ...
PMID:Ethanol is a potent stimulator of phosphatidylcholine breakdown in cultured rat hepatocytes. 173 64

Endogenous arginine vasopressin was previously shown to modulate the rate of loss of functional (CNS) tolerance to ethanol, suggesting that chronic ethanol ingestion might alter vasopressin synthesis and/or release. Since extrahypothalamic vasopressin is believed to be involved in the CNS effects of the peptide, we determined the effect of ethanol on vasopressin mRNA in the bed nucleus of the stria terminalis (BST), as well as in several hypothalamic nuclei. Chronic ethanol ingestion, that produced functional tolerance and physical dependence in mice, resulted in decreased vasopressin mRNA levels in all areas examined. In contrast, as expected, dehydration resulted in increases in vasopressin mRNA in the BST and in all hypothalamic nuclei except the suprachiasmatic nucleus. In the BST, both ethanol ingestion and dehydration affected cells in the central region of the nucleus, while cells in the caudal portion were only affected by ethanol treatment. The results indicate that chronic ethanol ingestion generally reduces the synthesis of vasopressin, and that increased vasopressin synthesis is not necessary in order for the peptide to affect ethanol tolerance.
 ...
PMID:Chronic ethanol ingestion decreases vasopressin mRNA in hypothalamic and extrahypothalamic nuclei of mouse brain. 174 46

To assess the chronic effect of ethanol on vasopressin release and synthesis, hypothalamic vasopressin mRNA, plasma vasopressin levels and plasma osmolality were measured in control rats and rats exposed chronically to ethanol by vapor inhalation for 8 days. The level of hypothalamic vasopressin mRNA (vasopressin synthesis) was unchanged or significantly decreased in ethanol-treated rats, even when these animals displayed increased plasma osmolality and vasopressin levels. The results suggest that chronic ethanol exposure produces a down-regulation of vasopressin synthesis and/or a disruption of vasopressin synthesis-secretion coupling. These findings may have important implications for evaluation of the hydration state of chronic alcoholics.
 ...
PMID:Chronic ethanol exposure uncouples vasopressin synthesis and secretion in rats. 177 24

The recent investigations on biochemical and biophysical mechanisms of ethanol in acute intoxication, tolerance and physical dependence suggest that the cell membrane, intracellular metabolism and central neurotransmitters are involved. In acute intoxication ethanol increases the "fluidity" of the cell membrane and stimulates the central gabergic system. In alcoholics, the body adapts, and in the presence of ethanol, the cell membrane becomes more "rigid" and the gabergic system hypoactive. When alcohol intake is discontinued the hypoactivity of the gabergic system is unmasked and it is manifested as withdrawal syndrome. The alcohol intake compensates for the clinical symptoms of decreased gabergic activity and thereby continuously prevent the onset of withdrawal symptoms. On the other hand, intact central noradrenergic and 5-hydroxytryptaminergic systems as well as the neuropeptide vasopressin maintain the tolerance. After withdrawal syndrome, membrane alterations and the state of diminished gabergic activity gradually return to normal. This period of slow recuperation corresponds to the subacute withdrawal syndrome. In this period, there is a continuous desire for alcohol intake. Further, alcoholics, in this situation, are very vulnerable with feelings of insecurity, fragility and isolation. All these factors additionally induce a latent desire for ethanol. It follows then that a stimulation of decreased gabergic activity is a new approach in drug therapy of alcoholism. One of these new stimulants is acamprosate. The new substance is a structural analogue of GABA and acts as an agonist on gabergic receptors. Therefore, acamprosate improves the central gabergic activity. Alcoholics treated with acamprosate stated that they no longer felt a desire for alcohol intake. In this way, acamprosate maintains the abstinence for several months during the post-withdrawal phase.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Modern drug therapy in alcoholism]. 180 68

The acute effects of ethanol on plasma atrial natriuretic peptide levels were investigated in 4 clinically healthy males, aged 24-26 years, consumed either 750 ml of water as a control study, or the same beverage with 1 ml/kg alcohol added, which increased the plasma alcohol concentration to 99.12 +/- 15.10 mg/dl at 60 min. Plasma atrial natriuretic peptide levels were significantly higher in the alcohol study compared to the control study at each time point (10, 20, 30, 60, 120 min after drinking onset), and with a peak at 10 min. Atrial natriuretic peptide levels showed a positive significant correlation with plasma antidiuretic hormone in the control group, while no relationship was found between the two peptides in the alcohol study. Moreover, a significant correlation exists between plasma atrial natriuretic peptide levels and systolic arterial blood pressure, and heart rate, and between the variations in atrial natriuretic peptide values and the variations in plasma sodium, serum ethanol, and plasma osmolality in the alcohol study. Acute ethanol intake causes an increase in urinary volume, and a decrease in urinary potassium excretion and urinary osmolality, and no change in urinary sodium excretion. These data suggest that acute ethanol administration causes a rapid increase in plasma levels of atrial natriuretic peptide, which could be an important factor of ethanol-induced diuresis. The main mechanisms for increased atrial natriuretic peptide release from atria after acute ethanol ingestion seem to be atrial stretch, due to the increase in arterial blood pressure, in heart rate, in sympathetic tone, and in plasma osmolality, and to a direct secretory effect by antidiuretic hormone.
 ...
PMID:A possible role of atrial natriuretic peptide in ethanol-induced acute diuresis. 182 57

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.
 ...
PMID:Ethanol causes desensitization of receptor-mediated phospholipase C activation in isolated hepatocytes. 184 16


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>