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)

Nocturia may be attributable to nocturnal polyuria (nocturnal urine overproduction), a diminished nocturnal bladder capacity or a combination of the two conditions.A disorder of the vasopressin (antidiuretic hormone) system with very low or undetectable levels of vasopressin at night, affecting some elderly people, may cause an increase in the nocturnal urine output, which in the most extreme cases accounts for 85% of the 24-hour diuresis. The increased urine output can be treated with desmopressin orally at bedtime, generally using low doses. Self-imposed fluid restrictions before bedtime are not effective in reducing the nocturnal urine output in this condition. Nocturia is also more prevalent in association with a reduced bladder capacity. Antimuscarinic drugs are used in attempts to depress involuntary bladder contractions. Decreased nocturnal voided volumes in men and consequent increased nocturia may suggest difficulty in emptying the bladder or detrusor overactivity. alpha(1)-Adrenoceptor antagonists and 5alpha-reductase inhibitors are often used in men with symptoms indicative of benign prostatic hyperplasia, and one of their effects is reduction of nocturia. In women, estrogen deficiency, a common consequence of the menopausal transition, causes atrophic changes within the urogenital tract. Consequently, such women are more disposed to having urogenital symptoms, among them nocturia. This review emphasises the importance of correctly diagnosing and treating nocturia in elderly patients. This will improve patients' sleep and, in turn, reduce their risk of fall injuries and the associated detrimental consequences, thereby improving patients' health and quality of life.
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PMID:Pharmacotherapy for nocturia in the elderly patient. 1743 26

Perfluorododecanoic acid (PFDoA), a synthetic perfluorinated chemical, has been detected in environmental matrices, wildlife, and human serum. Its potential health risk for humans and animals has raised public concern. However, the effects of chronic PFDoA exposure on male reproduction remain unknown. The aim of this study was to determine the effects of chronic PFDoA exposure (110 days) on testosterone biosynthesis and the expression of genes related to steroidogenesis in male rats. In this study, we examined the serum levels of sex hormones, growth hormone, and insulin in male rats. Testicular morphology and the expression of key genes and proteins in testosterone biosynthesis were also analyzed. Markedly decreased serum testosterone levels were recorded after 110 days of PFDoA exposure at 0.2mg PFDoA/kg/day and 0.5mg PFDoA/kg/day, and cast-off cells were observed in some seminiferous tubules in testes exposed to 0.5mg PFDoA/kg/day. PFDoA exposure resulted in significantly decreased protein levels of steroidogenic acute regulatory protein (StAR) and cholesterol side-chain cleavage enzyme (P450scc), along with significantly reduced mRNA levels of insulin-like growth factor I (IGF-I), insulin-like growth factor I receptor (IGF-IR), and interleukin 1alpha (IL-1alpha) in rat testes at 0.2mg/kg/day and 0.5mg/kg/day. In addition, PFDoA exposure also affected the expression of some genes in the hypothalamo-neurohypophyseal system. However, PFDoA did not affect the expression of 5alpha-reductase, 3alpha-hydroxysteroid dehydrogenase, or aromatase in testis and liver. These findings demonstrate that chronic PFDoA exposure disrupts testicular steroidogenesis and expression of related genes in male rats. Multiple factors may be involved in the inhibition of testosterone by PFDoA.
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PMID:Chronic exposure to perfluorododecanoic acid disrupts testicular steroidogenesis and the expression of related genes in male rats. 1939 62