Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasopressin (ADH) acts in humans mainly upon renal collecting tubules. By changing their water permeability it plays a key role in regulation of renal water excretion. Acting upon vascular smooth muscle cells, it causes vasoconstriction and raised arterial blood pressure. This hormone was also proven to cause constriction of cultured mesangial cels, it causes vasoconstriction and raised arterial blood pressure. This urea (Seldin, Giebisch 1985), to release the natriuretic hormone as well as to stimulate hepatic glycogenolysis (Abramov et al. 1987). The influence of vasopressin upon peritoneal transport of solutes was studied, too. ADH influenced the passage of phosphate and rubidium through the isolated rabbit mesentery (Berndt, Gosselin 1961) as well as sodium flux through isolated rabbit omentum (Shear et al. 1966). It caused the drop in urea dialysance in dogs subjected to peritoneal dialysis (Henderson et al. 1971). The subject of our study was the assessment of the action of the antidiuretic hormone under "in vitro" conditions upon the peritoneal transfer of urea, the solute present in human body fluids and removable by peritoneal dialysis.
Acta Med Pol 1989
PMID:Vasopressin-induced changes in permeability of peritoneal mesothelium for urea "in vitro". 248 58

With improved understanding of the pathophysiology of bacterial meningitis, a number of points in the deleterious inflammatory cascade have been identified as possible sites for modulation. Dexamethasone attenuates tissue injury by inhibiting host mediators at several steps in the inflammatory process. Animal and clinical trials have demonstrated that adjunctive corticosteroid therapy reduces the production of cytokines in the CSF. This results in decreased severity of the inflammatory process and fewer neurologic sequelae. However, routine use of steroids adjunctive treatment of bacterial meningitis remains controversial. Data support the use of adjunctive corticosteroid therapy in children with S. pneumoniae and H. influenzae type b meningitis. There is not sufficient evidence supporting the use of adjunctive corticosteroid therapy in patients with meningitis caused by N. meningitidis, which is the main cause of purulent meningitis in Poland. Also, the routine use of the dexamethasone in children and adult meningitis in Poland cannot presently be recommended. When using dexamethasone timing and dosage seems to be crucial. Administration before or with antibiotics is optimal for attenuating the subarachnoid space inflammatory response. The host's inflammatory response can be accompanied by the neuroendocrine response which is complex and its mediators are not well understood. Data indicate that the large component of the neuroendocrine response (e.g. inadequate secretion of ADH and large adrenocortical stress response) adversely affects the outcome from bacterial meningitis. So, the modulating effect of dexamethasone on both inflammatory and neuroendocrine response may be beneficial in bacterial meningitis and can probably be, achieved with sufficiently high dose of dexamethasone w has not yet been specified. Based on present pathophysiological and pharmacokinetic data, and to achieve maximum benefits and minimum complications, dexamethasone therapy started 10 min before the first dose of antibiotic and given every 12 h for only 2 days in a dose 0.8 mg/kg/day is suggested. Future studies of the pathogenesis and pathophysiology of bacterial meningitis may lead to the development of other adjunctive treatment strategies, improving the outcome of this serious disease.
Pol Merkur Lekarski 1997 Apr
PMID:[Supportive (antiinflammatory) treatment of bacterial meningoencephalitis with dexamethasone]. 937 71

Heavy alcohol consumption is associated with increased risk of cancers including digestive tract, liver, pancreas, colorectum and breast. Direct correlations between alcohol consumption and development of cancer are still unknown. The differences in activities of ADH and ALDH between cancer tissues and normal mucosa might be a factor for metabolic changes and disturbances in low- mature cancer cells, might be a reason for the high level of acetaldehyde and intensifying carcinogenesis. Moreover releasing ADH and ALDH from cancer cells can cause increase of these enzymes activities in the sera of patients with cancer.
Pol Merkur Lekarski 2008 Aug
PMID:[Alcohol dehydrogenase and aldehyde dehydrogenase in malignant diseases--Part II]. 1894 44

Diabetes insipidus is caused by insufficient secretion of vasopressin (ADH) or by an inability of the kidneys to respond to ADH. Pregnancy-associated DI occurs rarely but is connected with severe complications such as preeclampsia and hepatic function abnormalities. The following paper presents the case of a 36-year-old patient who had been diagnosed with diabetes insipidus in the 34th week of pregnancy.
Ginekol Pol 2011 Jul
PMID:[Diabetes insipidus in pregnancy--a case report]. 2191 33

Stress is generally a natural phenomenon that affects behaviour, physiological processes, and neuroendocrine, neurochemical, neurological and immune responses. Many somatic and mental disorders are thought to result from chronic stress. Stress-induced gonadal dysfunction is not restricted to humans, but is observed in all higher animals. Stress-induced gonadal dysfunction comprises disturbances of the hypothalamic-pituitary-gonadal axis and of spermatogenesis. Various stressors induce changes in the secretion of neurotransmitters and hormones, such as CRH, ADH, beta-endorphins, somatostatin, VIP, PRL, GH, TSH, dopamine, serotonin, neuropeptide Y, melatonin, ACTH, glucocorticosteroids, catecholamines and androgens. In acute stress, testicular function is principally modified by cytokines and fluctuating concentrations of gonadotropins, while in chronic stress, hypogonadotropic hypogonadism and disruption of spermatogenesis of varying severity, including spermatogenetic arrest, are observed. In spite of the decades-long interest in the relationships between psychological stress and the function of male gonads, many questions in this area remain unanswered.
Endokrynol Pol 2012
PMID:Psychological stress and the function of male gonads. 2237 97

Upregulation of Brf1 (TFIIB-related factor 1) and Pol III gene (RNA polymerase III-dependent gene, such as tRNAs and 5S rRNA) activities is associated with cell transformation and tumor development. Alcohol intake causes liver injury, such as steatosis, inflammation, fibrosis, and cirrhosis, which enhances the risk of HCC development. However, the mechanism of alcohol-promoted HCC remains to be explored. We have designed the complementary research system, which is composed of cell lines, an animal model, human samples, and experiments in vivo and in vitro, to carry out this project by using molecular biological, biochemical, and cellular biological approaches. It is a unique system to explore the mechanism of alcohol-associated HCC. Our results indicate that alcohol upregulates Brf1 and Pol III gene (tRNAs and 5S rRNA) transcription in primary mouse hepatocytes, immortalized mouse hepatocyte-AML-12 cells, and engineered human HepG2-ADH cells. Alcohol activates MSK1 to upregulate expression of Brf1 and Pol III genes, while inhibiting MSK1 reduces transcription of Brf1 and Pol III genes in alcohol-treated cells. The inhibitor of MSK1, SB-747651A, decreases the rates of cell proliferation and colony formation. Alcohol feeding promotes liver tumor development of the mouse. These results, for the first time, show the identification of the alcohol-response promoter fragment of the Pol III gene key transcription factor, Brf1. Our studies demonstrate that Brf1 expression is elevated in HCC tumor tissues of mice and humans. Alcohol increases cellular levels of Brf1, resulting in enhancement of Pol III gene transcription in hepatocytes through MSK1. Our mechanism analysis has demonstrated that alcohol-caused high-response fragment of the Brf1 promoter is at p-382/+109bp. The MSK1 inhibitor SB-747651A is an effective reagent to repress alcohol-induced cell proliferation and colony formation, which is a potential pharmaceutical agent. Developing this inhibitor as a therapeutic approach will benefit alcohol-associated HCC patients.
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PMID:Mitogen- and Stress-Activated Protein Kinase 1 Mediates Alcohol-Upregulated Transcription of Brf1 and tRNA Genes to Cause Phenotypic Alteration. 3268 86