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)

Chronic exposure of mice to ethanol leads to the development of functional tolerance to the hypothermic and sedative effects of this drug. Treatment of the animals with the mammalian antidiuretic hormone, arginine vasopressin, results in a prolonged duration of such tolerance, in comparison to animals exposed to ethanol but not to the hormone. Another neurohypophyseal hormone, oxytocin, at an equimolar dose, is ineffective in maintaining tolerance. The centrally mediated effects of arginine vasopressin on memory processes may be related to the hormone-induced prolongation of ethanol tolerance.
Drug Alcohol Depend
PMID:Peptide--neurotransmitter interactions influencing ethanol tolerance. 52 81

The mechanisms underlying the frequent association of nausea and vomiting with elevations of plasma vasopressin(PAVP) were studied in man and rat. After oral water loads (N = 16), plasma osmolality fell in all human subjects and was associated with a decline in PAVP in 14 asymptomatic human subjects. In 2 human subjects, nausea occurred and was associated with increases in PAVP, without changes in blood pressure. During ethanol infusion (N = 28), PAVP was suppressed unless nausea supervened. In 4 nauseated human subjects, PAVP escaped from ethanol inhibition and rose to levels 10 times basal, despite the absence of hemodynamic changes. Apomorphine, a potent dopamine agonist and emetic agent, was administered to human volunteers in doses of 7 to 24 microgram/kg. There was no increase in PAVP in 3 human subjects who remained asymptomatic (7 to 16 microgram/kg). Ten human subjects experienced nausea after 16 microgram/kg, which was followed shortly by marked increases in PAVP. Emesis occurred in 5 human subjects given 16 to 24 microgram/kg, and was followed by PAVP levels similar to those seen with nausea alone. In 7 human subjects from the nausea group, the repeat study (16 microgram/kg) after pretreatment with dopamine antagonist (haloperidol, N = 4; fluphenazine, N = 3) resulted in complete blockage of apomorphine-induced AVP release. In rats, which lack an emetic reflex, apomorphine doses of 200 microgram/kg induced only slight increases in PAVP when compared to the response to 16 microgram/kg in man. These studies indicate that stimulation of the emetic reflex results in AVP-release in man. Nausea-mediated AVP release supervenes over concomitant osmolar or pharmacologic (ethanol) inhibition.
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PMID:Influence of the emetic reflex on vasopressin release in man. 54 11

The classical areas for arginine-vasopressin (AVP) synthesis are the magnocellular supraoptic (SON) and paraventricular nuclei. More recently AVP was also demonstrated in neurons of the parvocellular suprachiasmatic nucleus (SCN) of the rat. This result was substantiated in the present study by means of immunoelectron microscopy, by subjecting sections to antivasopressin plasma. Conventional electron microscopy revealed dense-core vesicles in the SCN cell bodies and fibres (mean diameter 94.7 +/- 0.9 nm and 84.0 +/- 1.1 nm respectively). These vesicles were infrequent within the cell bodies and could not be accumulated by ethanol administration. Immunoelectron microscopy showed a positive reaction in the cell bodies and fibres within vesicles of 96.7 +/- 1.1 nm and 98.5 +/- 1.1 nm and 98.5 +/- 1.2 nm respectively. By comparison, the cell bodies and fibres of the SON showed immunoreactive granules of 143.0 +/- 1.8 and 147.3 +/- 1.8 nm respectively. The presence in the SCN of AVP in vesicles of different size than those in the SON suggests that synthesis of this substance is indeed occurring within the SCN cells.
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PMID:Immunoelectronmicroscopic localization of vasopressin in the rat suprachiasmatic nucleus. 71 7

Previous studies on intact and isolated blood vessels indicate that ethanol can exert depressant actions on vascular smooth muscle. This study, using isolated rat aortic strips and portal veins, was designed to ascertain whether acetaldehyde (ACT), a major metabolite of ethanol, could exert similar effects. The results indicate that ACT can: (a) inhibit spontaneous mechanical activity and lower baseline tension in aortic strips; (b) depending upon concentration, enhance (abolished by phentolamine) or inhibit such spontaneous contractions in portal veins; (c) dose-dependently attenuate contractions induced by epinephrine, vasopressin, serotonin and KCl; (d) cause non-competitive displacement of the contraction--effect curves of these vasoactive compounds; (e) relax drug-induced contractions of aortic and venous smooth muscle, (f) attenuate Ca2+-induced contractions of K+-depolarized aortas and portal veins. These profound depressant actions of ACT are not attenuated, prevented or mimicked by alpha-adrenergic histaminergic, cholinergic, or serotonergic blocking drugs, nor are they attributable to actions on beta-adrenoreceptors, or release of prostaglandin-like substance. The direct vasodepressant actions of ACT on vascular smooth muscles may play significant roles in alcohol-induced peripheral vasodilatation and hypotension, and cardiovascular collapse noted in the alcohol-Antabuse reaction.
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PMID:Acetaldehyde on vascular smooth muscle: possible role in vasodilator action of ethanol. 72 Mar 89

Rats were trained to accept ethanol in their drinking water, by successive small increments or decrements in alcohol concentration in response to the individual consumption of each rat. Those injected with desglycinamide9-lysine8-vasopressin (DGLVP), 1--4 microgram SC every second day, attained almost twice as high a final acceptance concentration (FAC) and mean daily ethanol intake (g/kg) as vehicle-treated controls. Hypophysectomized animals initially accepted the same alcohol concentrations as intact rats, but drank much larger volumes and correspondingly higher daily g/kg intakes. However, this was rapidly succeeded by rejection of all but very low concentrations, which was unaffected by DGLVP. During a subsequent free-choice period (water vs. ethanol at individual FACs), the groups maintained their relative positions with respect to ethanol intake. This was not altered by injection of vasopressin in the hypophysectomized rats, but was overcome by raising the alcohol concentration. The results suggest that vasopressin-like peptides facilitate acquisition of alcohol drinking behavior.
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PMID:Effect of vasopressin-like peptides on consumption of ethanol by the rat. 73 31

The responses of isolated smooth muscle tissues to the polypeptides oxytocin, vasopressin and bradykinin were evaluated in the presence of the tetrahydroisoquinoline salsolinol. Significant antagonism occurred to oxytocin and vasopressin while the effects of bradykinin were unaltered. These results suggest that the in vivo formation of salsolinol after ethanol consumption could have significant physiological consequences.
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PMID:Antagonism of smooth muscle responses to oxytocin and vasopressin by salsolinol. 89 6

1. A method is described for the serial determination of renal tubular reabsorption of amino acids in the ethanol-anaesthetized rat. It utilizes intravenous radio-labelled inulins, automated amino acid analysis and forced diuresis. 2. Intravenous loading with phenylalanine and infusion of phenylalanine analogues in this preparation decrease reabsorption of endogenous amino acids in accordance with existing concepts of amino acid transport. 3. Maximal tubular reabsorption (Tmax) could not be demonstrated for phenylalanine at plasma concentration below 9 mmol/l. 4. Infusion of phenylalanine analogues into phenylalanine-loaded ('phenylketonuric') rats did not specifically inhibit tubular reabsorption of phenylalanine and it is unlikely that any of the substances tested have a potential therapeutic use in man. 5. p-Guanidino derivatives of phenylalanine, in contrast to p-amino derivatives, appear to cause a dose-related basic aminoaciduria. 6. Consideration of urinary flow rates and sodium excretion suggests that the ethanol anesthesia does not modify amino acid reabsorption through effects on sodium transport or antidiuretic hormone.
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PMID:Effects of phenylalanine analogues on renal tubular reabsorption of amino acids in the rat. 91 60

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

Neurophysiological, neurochemical and behavioral studies of the effects of ethanol on the nervous system have so far failed to identify specific, direct, primary mechnisms of action that may account for the typical pattern of alcohol intoxication in vivo. Electroencephalogram and evoked response studies indicate biphasic effects in the intact subject, which may correlate better with the level of arousal than with a specific drug action. Effects on spinal reflexes are also biphasic, probably representing the net result of direct influence on resting membrane potential, primary afferent depolarization, and neurotransmitter release. With the exception of its inhibitory effect on release of oxytocin, vasopressin and possibly other hypothalamic peptides, ethanol does not appear notably different in its spectrum of effects from a wide range of other hypnotics, anesthetics and minor tranquilizers. Interpretation of the findings is complicated by the fact that functional alteration of any given neuronal system by ethanol in vivo may reflect a) direct local action of ethanol on the cells under study, b) change in the input to those cells because of an action elsewhere in the nervous system, c) effects of ethanol metabolites, or d) indirect consequences of decreased blood flow, oxygen or metabolite supply, hormonal action, or hypothermia, due to disturbances of homeostasis in the whole body as a result of deep intoxication. To date, attempts to circmvent b, c and d by the study of brain tissue in vitro have shown consistent effects of ethanol only at concentrations well above those that are meaningful in vivo. Relatively specific patterns of action of different drugs in vivo may prove to be largely dependent on their customary rates and routes of administration, and on summation of minor differences in the dose-response curves with different types of neuron, even though the basic types of molecular action may be essentially similar.
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PMID:Direct effects of ethanol on the nervous system. 109 39

A sensitive and specific double antibody radioimmunoassay has been developed capable of measuring LH-RH in extracted human plasma. Thyrotropin releasing hormone, lysine vasopressin and most of LH-RH analogues did not appear to affect the assay. Hypothalamic extract and some of the LH-RH analogues produced displacement curves which were parallel to that obtained with the synthetic LH-RH. Sensitivity of the radioimmunoassay was about 3 pg per assay tube. The coefficient of variation of intraassay was 6.4%, while that of interassay was 9.6%. Exogenous LH-RH could be quantitatively extracted by acidic ethanol when varying amounts of synthetic LH-RH were added to plasma. Immunoreactivity of LH-RH was preserved in plasma until 2 hr in the cold and gradually reduced thereafter. The plasma levels in LH-RH were 20 pg/ml or less in normal adults and not detectable in children. The aged males over 60 yr and postmenopausal women showed a tendency to have higher levels of plasma LH-RH. Plasma LH-RH level was significantly higher in midcycle than in follicular and luteal stages. The disappearance rate of LH-RH from the circulation after intravenous injection could be represented as half times of 4-6 min. Between 0.2-0.4% of the injected dose was excreted into urine within 1 hr. These results indicate that the determination of LH-RH might be a useful tool for elucidating hypothalamic-pituitary-gonad interactions.
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PMID:Radioimmunoassay for luteinizing hormone releasing hormone in plasma. 110 Mar 64


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