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 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

Eighty-eight patients with craniocerebral trauma were studied prospectively to assess the effects of the injury on sodium and water balance. Abnormalities of serum sodium and osmolality occurred in 11 of the 76 patients who were on the study more than 24 hours, and the incidence of these abnormalities was directly related to the severity of the craniocerebral injury. Hyponatremic hypo-osmolar states were as frequent as were hypernatremia and serum hyperosmolality. The major cause of the hyponatremia was inappropriate antidiuretic hormone secretion; hypernatremia was due to dehydration and occurred predominantly in comatose patients with increased insensible fluid losses associated with pyrexia. We recommend that the initial fluid intake after craniocerebral trauma be kept between 1500 and 1800 ml/24 hours and that further fluid management be dictated by repeated serum electrolyte determinations. The electrolyte balance should be monitored continuously after a significant head injury for up to 2 weeks, because hyponatremic states sometimes develop more than 1 week after injury. The serum alcohol was measured on admission, and the level of serum alcohol correlated well with the serum osmolality on admission; thus, the degree of elevation of serum osmolality was a very good guide to the serum alcohol level. However, there was no statistically significant correlation between alcohol intoxication or chronic alcoholism and the late development of serum sodium and osmolality disturbances.
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PMID:Metabolic disturbances after head injury: abnormalities of sodium and water balance with special reference to the effects of alcohol intoxication. 68 1

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

Eighty-six intracranial cannula placements in 51 rats were tested with unilateral, 2-mul injections of a 0.60-osmol/kg solution, sucrose dissolved in isotonic sodium chloride. To assess antidiuretic hormone (ADH) release, a water diuresis was induced and spontaneous urinations were collected and analyzed for sodium by flame photometry. On alternate test days the 0.60-osmol/kg solution was injected into sleeping rats, and latencies to drink and volume drunk were recorded. Injections at 42 placements elicited neither drinking nor adtidiuresis on two separate test days each; at 15, both antidiuresis and drinking on at least two of three tests each; at 19, drinking but not antidiuresis; at 10, antidiuresis but not drinking. Positive drinking and ADH placements were not distinctly separated. They clustered in the bed nucleus of the stria terminalis, the preoptic areas, and the anterior portions of the hypothalamus. Placements in the medial forebrain bundle and dorsal to the anterior hypothalamic area elicited thirst but not ADH release for the most part. Placements nearest the supraoptic nucleus were weak or negative for ADH release. Central nervous system osmo-receptors exist and seem not to be the neurosecretorycells. Thirst osmoreceptors and antidiuretic osmoreceptors seem to be contiguous, but distinct.
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PMID:Localization of thirst and antidiuretic osmoreceptors by intracranial injections in rats. 113 May 53

Two experiments were carried out to investigate the responses of sheep (N = 6) to intracerebroventricular (ICV) injections of atriopeptin III [atrial natriuretic factor (5-28), AP III]. In Experiment, 1, 24-h dehydrated animals were given 0 (saline vehicle control), 10 or 30 micrograms AP III directly before the presentation of water. The highest dose of AP III significantly (p less than 0.02) reduced the amount of water drunk in the subsequent 20 min. In Experiment 2, blood samples were taken at various intervals before and after ICV injection of 0 or 30 micrograms AP III when the sheep were water replete or 24-h dehydrated. Plasma concentrations of vasopressin (AVP) and cortisol were measured and estimates were made of plasma osmolality. In the dehydration condition, AVP levels were somewhat reduced (p less than 0.059) after AP III administration but no decrease was observed when the animals were euhydrated. No significant changes in plasma osmolality or cortisol concentrations were observed in response to AP III or the saline vehicle. Because a large dose of AP III (30 micrograms ICV) was required to produce the comparatively small behavioral and endocrine effects observed in this study, the results are suggestive of a pharmacological, rather than a physiological, action of the peptide in this species.
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PMID:Centrally administered atriopeptin III reduces water intake and vasopressin secretion in dehydrated sheep. 182 82

Intracerebroventricular (ivt) angiotensin II (ANG II) at 0.4, 2, 10, and 50 ng.kg-1.min-1 increased arterial pressure in conscious sheep in a dose-related manner (26 mmHg, P less than 0.05, at 50 ng.kg-1.min-1). Total peripheral resistance (TPR) and right atrial pressure also increased. Heart rate, stroke volume, and cardiac output did not change. Pressor responses to ivt ANG II were not caused by leakage of ANG II into the periphery, because plasma concentrations of ANG II did not change from control (31 +/- 7 pg/ml) at the highest dose of ANG II infused. In contrast, intravenous (iv) ANG II, 10 and 50 ng.kg-1.min-1, increased arterial pressure 29 and 47 mmHg, respectively (P less than 0.05), and decreased heart rate. ANG II, 10 ng.kg-1.min-1 iv, increased plasma ANG II levels from 36 +/- 6 to 354 +/- 69 pg/ml (P less than 0.05). Intracarotid (ic) ANG II, 10 ng.kg-1.min-1, increased arterial pressure 31 mmHg (P less than 0.05) but did not alter heart rate. ANG II ivt caused a dose-related drinking response, with a positive correlation between the amount of water drunk during ivt ANG II infusion and the increase in arterial pressure. Infusions of ANG II at 50 ng.kg-1.min-1 ivt were associated with decreased plasma osmolality and potassium concentration and increased plasma vasopressin concentration.
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PMID:Hemodynamic and behavioral effects of angiotensin II in conscious sheep. 233

Angiotensin II (AII; 300 ng) injected into the lateral cerebral ventricle produced significant drinking responses and also stimulated release of lysine vasopressin (LVP) in conscious, water replete, unrestrained minipigs. Plasma LVP concentration, measured by a specific radioimmunoassay, was decreased by drinking. At the end of the experiment the level was inversely proportional to the volume of water drunk in response to the AII, and not to changes in plasma osmolality. These findings suggest that AII-stimulated LVP release is influenced by a negative feed-back mechanism, probably involving oropharyngeal receptors.
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PMID:Drinking and vasopressin release following central injections of angiotensin II in minipigs. 272 48

A 52-year-old man, known to be alcohol dependent, was admitted to hospital because of intense drowsiness. He had previously drunk over 100 g alcohol daily, but for the last 2 days "not a drop". Serum sodium concentration was 103 mmol/l, serum osmolarity was low (216 mosmol/l) and urine osmolarity remarkably high (373 mosmol/l). These abnormalities, taken in conjunction with his normal water balance (absence of obvious edema or dehydration), suggested the diagnosis of inappropriate secretion of antidiuretic hormone (ADH), and this was confirmed by a water loading test. Exclusion of the recognized causes of inappropriate ADH secretion left alcohol withdrawal as the only tenable explanation. The reabsorption of water which it induced was the cause of the patient's hyponatraemia and drowsiness. Restriction of fluid intake to 500 ml daily with continued total abstinence from alcohol led to rapid recovery. The discovery of hyponatraemia in an alcoholic in a state of normal water balance should rouse suspicion of inappropriate ADH secretion.
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PMID:[Inappropriate ADH secretion caused by alcohol withdrawal: a rare cause of hyponatremia]. 280 92

The concurrent cardiovascular and dipsogenic effects produced by i.c.v. administration of angiotensin II (AII) have been investigated in vasopressin-deficient (Brattleboro) and control (Long-Evans) rats. When animals were allowed to drink during testing, the pressor effect of i.c.v. AII (500 ng) in Long-Evans rats (26 +/- 3/26 +/- 3 mm Hg) was significantly greater than that produced when drinking water was not available (19 +/- 2/18 +/- 2 mm Hg). There was a significant decrease in heart rate only when water was available. There was no pressor response to i.c.v. AII in Brattleboro rats not allowed to drink, whereas blood pressure increased by 17 +/- 3/14 +/- 1 mm Hg in response to i.c.v. AII when drinking water was present. There were no significant changes in heart rate following i.c.v. AII in Brattleboro rats. When baseline drinking was taken into account, Brattleboro rats still drank significantly more water than Long-Evans rats in response to i.c.v. AII. Pretreatment of Long-Evans rats with the V1 vasopressin antagonist, D(CH2)5Tyr(Et)DAVP, decreased the pressor effect of i.c.v. AII to a level not significantly different from that of Brattleboro rats allowed to drink. Under these conditions the amount drunk by Long-Evans rats was not significantly less than that drunk by Brattleboro rats. These results confirm that the central pressor actions of AII are mediated, in part, by release of vasopressin and suggest that the greater dipsogenic effect of i.c.v. AII in Brattleboro compared with Long-Evans rats may be due, partly, to its lesser pressor activity in these animals.
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PMID:Cardiovascular and dipsogenic effects of angiotensin II administered i.c.v. in Long-Evans and Brattleboro rats. 341 93

The roles of antidiuretic hormone (ADH) and aldosterone in the elicited diuretic responses of trained and untrained men to seated, supine, and head-out water immersed conditions were studied. Volunteers were comprised of groups of six untrained individuals, six trained swimmers, and six trained runners. Each subject underwent three protocols, six hours in a seated position, supine position, or immersion (35 degrees C water). The last two protocols were preceded and followed by 1 h of seated position. After 10 h of fasting, 0.5% body wt of water was drunk. One hour later the trained groups had higher urine osmolalities (P less than 0.05) and urinary excretion rates of ADH (P less than 0.05) and lower urine flow rates (P less than 0.05) than untrained subjects. Throughout the sitting protocol, urinary ADH was also higher in both trained groups (P less than 0.05). Both supine posture and immersion resulted in significant decreases in urinary ADH in the untrained subjects (P less than 0.05) but no changes wer noted in swimmers and only during the second hour of immersion in the runners (P less than 0.05). The natriuresis and kaliuresis were greater during immersion than in the supine position but plasma renin activity, measured only in trained groups, and plasma aldosterone, measured in the untrained group, were decreased similarly with both protocols. The increases in urinary sodium excretion and urine flow rate were lower in trained than untrained subjects during the supine and immersion protocols (P less than 0.05). The data are compatible with an increased osmotic but decreased volume sensitivity of ADH control in trained men.
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PMID:Fluid conservation in athletes: responses to water intake, supine posture, and immersion. 352 6


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