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)

Primary nocturnal enuresis is common and has considerable psychological ramifications for children as they get older. It is a familial condition with complex inheritance patterns. The pathophysiology of the condition appears to be related to poor arousal from sleep, nocturia due to deficient vasopressin release in sleep and possibly a decrease in functional bladder capacity especially at night. The mainstay of treatment is the bed-wetting alarm. In recent years, desmopressin nasal spray has found a clinical niche as a short-term solution for children attending school camps or sleeping over at friends' houses and as treatment in the medium term for those unresponsive to treatment with a bed-wetting alarm. It may also be used as an adjunct to the use of the alarm. Treatment with imipramine is increasingly in disfavour because the relapse rate is unacceptably high and fatal overdose is a real possibility.
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PMID:Nocturnal enuresis: what is happening? 1072 98

Nocturnal polyuria is common in the elderly. In this condition the normal circadian rhythm of urine production is reversed so that urine flow is higher at night than during the day. Elderly men with nocturnal polyuria are commonly referred for prostate surgery, which, not surprisingly, fails to relieve their symptoms. Compared with controls, patients with nocturnal polyuria have higher nocturnal sodium excretion but not higher nocturnal free-water clearance. Similar results have been obtained in children with nocturnal enuresis. Use of vasopressin analogues to induce water retention in elderly patients with nocturnal polyuria is illogical and potentially hazardous; nocturia can be more safely alleviated by diuretic therapy. Nocturnal polyuria in the elderly is associated with hypertension: this is consistent with studies in younger age groups that show that essential hypertension is associated with nocturia and with increased night/day ratios for sodium excretion. We propose that nocturnal polyuria and essential hypertension share some of the same pathophysiological determinants. Specifically, we suggest that a defect in the nitric-oxide pathway may lead to resetting of the pressure-natriuresis relation in the kidney, sodium retention, and compensatory nocturnal natriuresis. This suggestion is consistent with evidence that ageing and essential hypertension are both associated with defects in the nitric-oxide pathway. Our hypothesis has obvious therapeutic implications. More generally, studying the pathogenesis of nocturnal polyuria in the elderly may advance our understanding of the pathogenesis of essential hypertension.
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PMID:Relation of nocturnal polyuria of the elderly to essential hypertension. 1084 Nov 44

Polyuria is defined as the passage of large volumes of diluted urine secondary to an abnormality of urine concentration. This disorder can result either from deficient secretion of vasopressin (cranial diabetes insipidus), or from renal resistance to vasopressin (nephrogenic diabetes insipidus), primary polydipsia, osmotic diuresis, electrolytic disorders or drugs. Suspicion of impaired renal concentration ability can be confirmed by a fluid deprivation test. The administration of exogenous vasopressin allows to clarify the pathogenetic mechanism. Once the mechanism responsible for polyuria has been clarified it is mandatory to search for underlying causes. Treatment of polyuria should be causal, if its origin is known, and/or symptomatic in order to prevent severe dehydration. Symptomatic treatment of cranial diabetes insipidus consists of administering exogenous vasopressin. Salt restriction associated to a combined administration of hydrochlorothiazide/amiloride or hydrochlorothiazide/indomethacin can reduce urine output by 20 to 50% in case of nephrogenic diabetes insipidus. Pollakiuria is defined as a daytime urinary frequency. It can be isolated or may be a manifestation of lower urinary tract infections, bladder instability, nephrolithiasis or concentrated acidic urines. Detailed history and physical examination represent major clues to diagnostic. Therapy of pollakiuria can be causal or symptomatic using anticholinergic drugs or reeducation in case of bladder instability. Nocturia is characterized by voluntary nocturnal micturitions secondary to conditions inducing impaired renal concentration ability, or to heart failure.
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PMID:[Polyuria, pollakiuria, and nocturia in children: diagnostic and therapeutic approach]. 1134 16

Although nocturnal voiding is frequently attributed to urologic disorders, nocturia and enuresis are also important symptoms of sleep-disordered breathing. However, polyuria can be elicited by obstructive sleep apnea as well as bedrest, microgravity and other experimental conditions where the blood volume is shifted centrally to the upper body. The nocturnal polyuria of sleep apnea is an evoked response to conditions of negative intrathoracic pressure due to inspiratory effort posed against a closed airway. The mechanism for this natriuretic response is the release of atrial natriuretic peptide due to cardiac distension caused by the negative pressure environment. This cardiac hormone increases sodium and water excretion and also inhibits other hormone systems that regulate fluid volume, vasopressin and the rennin-angiotensin-aldosterone complex. Treatment of sleep apnea and airway compromise has been shown to reverse nocturnal polyuria and thereby reduce or eliminate nocturia and enuresis. Thus, careful evaluation of nocturia and enuresis for evidence of nocturnal polyuria can increase the diagnostic certainty of referring primary care providers and sleep specialists. In addition, the resolution of these bothersome symptoms after treatment can contribute to patient satisfaction as well as reinforce treatment compliance.
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PMID:Sleep disordered breathing and nocturnal polyuria: nocturia and enuresis. 1457 73

Nocturia is a common symptom in the elderly, which profoundly influences general health and quality of life. One consequence of nocturia is sleep deterioration, with increased daytime sleepiness and loss of energy and activity. Accidents, e.g., fall injuries, are increased both at night and in the daytime in elderly persons with nocturia. Nocturia is caused by nocturnal polyuria, a reduced bladder capacity, or a combination of the two. Nocturnal polyuria can be caused by numerous diseases, such as diabetes insipidus, diabetes mellitus, congestive heart failure, and sleep apnoea. In the nocturnal polyuria syndrome (NPS), the 24-h diuresis is normal or only slightly increased, while there is a shift in diuresis from daytime to night. NPS is caused by a disturbance of the vasopressin system, with a lack of nocturnal increase in plasma vasopressin or, in some cases, no detectable levels of the hormone at any time of the 24-h period. The calculated prevalence of NPS is about 3% in an elderly population, with no gender difference. In NPS, there are serious sleep disturbances, partly due to the need to get up for micturition, but there is also increased difficulty in falling asleep after nocturnal awakenings and increased sleepiness in the morning. The treatment of NPS may include avoidance of excessive fluid intake, use of diuretics medication in the afternoon rather than the morning, and desmopressin orally at bedtime.
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PMID:Nocturia, nocturnal polyuria, and sleep quality in the elderly. 1517 8

Desmopressin is a synthetic vasopressin analogue mainly used in treatment of diabetes insipidus and nocturia. Studies in rats have revealed a sex difference in the response to a vasopressin infusion, which was diminished after treatment with an NSAID. This study was performed in man to investigate the influence of sex and concomitant treatment of piroxicam on the pharmacokinetics and dynamics of desmopressin, and to validate a previously described indirect response model. Eight healthy males and eight healthy females participated in the trial, which was conducted in a pharmacokinetic (PK) part followed by a pharmacodynamic (PD) part. Desmopressin was administered intravenously as a single dose (PK = dose 2 microg, PD = dose 0.2 microg). Piroxicam was administered to achieve steady state. The pharmacokinetic parameters of desmopressin were estimated and calculated by means of two-compartmental analysis. In the dynamic part a study design based on an oral hydration model was used. Parameters for urine flow and urine osmolality were estimated. Individual estimates of the pharmacokinetic parameters served as input to the indirect response model that subsequently was fitted to urine osmolality data. The pharmacokinetics of desmopressin after a fixed bolus injection was neither influenced by piroxicam nor sex of the subject. The pharmacodynamics of desmopressin showed a sex difference where females exhibited a more pronounced antidiuretic effect than males, which was statistically significant when the effects were submaximal (>4.5 h after dose). The sex differences were diminished after pre-treatment with piroxicam, indicating a prostaglandin PGE(2)-mediated mechanism. The indirect response model was confirmed, although the modelling could not distinguish a sex difference, indicating a limitation of this model compared with traditional descriptive statistics.
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PMID:A pharmacokinetic and pharmacodynamic study of desmopressin: evaluating sex differences and the effect of pre-treatment with piroxicam, and further validation of an indirect response model. 1552 45

Desmopressin, a synthetic antidiuretic hormone analogue, is the only drug currently approved for the treatment of nocturia associated with nocturnal polyuria or multiple sclerosis (MS). Compared with vasopressin, desmopressin has a longer lasting and more potent antidiuretic effect and is devoid of vasopressor and uterotonic effects. In two large, randomised, double-blind phase III trials in adults with nocturia associated with nocturnal polyuria, 3 weeks of oral desmopressin therapy was significantly more effective than placebo in reducing the mean number of nocturnal voids and in normalising the rate of nocturnal urine production. Beneficial effects of desmopressin on nocturia were maintained and increased in patients completing 10 or 12 months of further treatment in a nonblind extension of short-term trials. In randomised, double-blind trials in MS patients with nocturia, nasal desmopressin reduced the mean number of nocturnal voiding episodes by 31-54%. In both patient populations, desmopressin increased the initial sleep period or mean maximum period of uninterrupted sleep by approximately 2 hours, an outcome significantly greater than that achieved with placebo. In trials of < or =6 weeks duration in adults with nocturia, desmopressin was generally well tolerated. Most desmopressin-related adverse events were transient and mild or moderate in severity. Clinically significant hyponatraemia was reported in approximately 5% and required withdrawal from studies in < or =3% of patients.
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PMID:Desmopressin: in adults with nocturia. 1561 55

Nocturia is a common condition in the elderly that profoundly influences general health and quality of life. It appears to predict a higher risk of death. One consequence of nocturia is sleep deterioration, with increased daytime sleepiness and loss of energy and activity. Accidents, e.g. falls, are increased both at night and during the day in elderly persons with nocturia. Nocturia is caused by nocturnal polyuria, reduced voided volumes, or a combination of the two. Nocturnal polyuria can be caused by numerous diseases, e.g. diabetes insipidus, diabetes mellitus, congestive heart failure, and sleep apnoea. A disorder of the vasopressin system, with very low or undetectable vasopressin levels at night, is manifested as an increased nocturnal urine output, which in the most extreme cases reaches 85% of the 24-h diuresis: the prevalence of low or undetectable vasopressin levels at night has been estimated to be 3-4% in those aged >or= 65 years. Treatment of nocturia may include avoiding excessive fluid intake and use of diuretic medication in the afternoon rather than the morning, oral desmopressin at bedtime in cases of nocturnal polyuria, and antimuscarinic agents in the case of overactive bladder or impaired storage capacity of the bladder.
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PMID:Nocturia in relation to sleep, health, and medical treatment in the elderly. 1608 52

The circadian rhythm of urine formation was studied in younger (27 +/- 8 yr) and aged (76 +/- 3 yr) males. In 11 younger healthy examined persons a decrease of diuresis during the night as compared with the day time was due to a rise of solute free water reabsorption. In 31 aged males the change of the urine formation rhythm with increase of the nocturnal diuresis is based on a rise of osmolal clearance combined with an increase of the solute free water reabsorption. It is shown that blockade of autacoid secretion leads to normalization of the diuresis circadian rhythm. In 10 aged men, nocturia was due to a decrease of vasopressin secretion which resulted in a decrease of the solute free water reabsorption and an increase of diuresis. The obtained data are considered as an evidence for the role of renal autacoids, alongside with vasopressin, in regulation of the circadian rhythm of the kidney function.
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PMID:[Study of autacoids role in the regulation of circadian rhythm of the human renal function]. 1640 43

Primary nocturnal enuresis (PNE) is a common problem in childhood and adolescence. Although various treatments are highly effective, a common underlying hypothesis on the pathogenesis is lacking. The success of desmopressin, a synthetic analogue of the antidiuretic hormone vasopressin, has been attributed to increased renal water reabsorption that is mediated by activation of the renal vasopressin V2 receptor (V2R). However, this effect does not explain other symptoms of PNE, such as the failure to arouse upon bladder distension. This study identified a family in which one child displayed PNE and coexisting nephrogenic diabetes insipidus, as a result of a novel nonsense mutation in the V2R gene (C358X). Cell-biologic investigations revealed that V2R-C358X is retained in the endoplasmic reticulum and is unstable, which explains his nephrogenic diabetes insipidus. Consistently, extrarenal V2R-mediated responses were absent in the patient who was treated with desmopressin. Administration of desmopressin, however, changed his PNE into nocturia, because he now still voided unchanged high urinary volumes at night but woke up and went to the bathroom. Withdrawal of desmopressin was accompanied by bedwetting, whereas reintroduction again relieved the symptoms. Therefore, these data indicate that neither a functioning renal concentration system nor a functional V2R is needed for the therapeutic benefit of desmopressin in PNE. Rather, it suggests that another vasopressin receptor and other organ(s) is the target for desmopressin to relieve PNE.
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PMID:Relief of nocturnal enuresis by desmopressin is kidney and vasopressin type 2 receptor independent. 1738 37


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