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)

We have previously suggested that inhibition of renin release by sodium chloride is related to absorptive chloride transport in the loop of Henle. Infusion of sodium chloride fails to inhibit renin release in the adrenalectomized (Adx) rat, and dexamethasone restores renin responsiveness to sodium chloride. The purpose of the present study was to evaluate the relationship between loop function (urinary diluting and concentration capacity) and plasma renin concentration (PRC) in the Adx rat. After hypotonic sodium chloride infusion, free water clearance (CH2O) of Adx rats (0.56 ml/hr/100 g +/- 0.17 SE) was decreased (p less than 0.01) compared to controls (2.86 ml/hr/100 g +/- 0.29 SE); PRC of Adx rats (61.9 units/ml +/- 11.2 SE) was increased (p less than 0.01) above controls (6.0 units/ml +/- 1.7 SE). These differences persisted after administration of d(CH2)5Tyr(Et)VAVP, a potent ADH antagonist. In separate groups of animals, after water deprivation, urine concentration of Adx rat (1,401 mOsm/kg +/- 45 SE) was less (p less than 0.01) than that of controls (2,117 mOsm/kg +/- 169 SE). Dexamethasone normalized both CH2O and urinary concentrating ability and also decreased PRC in Adx rats. Thus, in the glucocorticoid deficient rat, increased renin release is associated with impaired loop function. The loop defect may account for high PRC that is not suppressed by sodium chloride.
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PMID:Mechanism of increased renin release in the adrenalectomized rat. Adrenal insufficiency and renin. 633 60

Micropuncture experiments, performed on adrenalectomized rats disclosed an impairment of the hypertonic sodium chloride transport of the thick ascending limb of Henle's loop (the diluting segment). This transport inhibition was documented by a delayed time course of NaCl-concentration decrease within the diluting segment. Assuming a pump leak model of the hypertonic NaCl-transport, we calculated a 50% inhibition of the NaCl-transport velocity compared with controls. Dexamethasone treatment for 3 days led to a normalization of the impaired transport velocity. Both, the reduced GFR as well as the impaired free water clearance are functionally linked to the diminished transport capacity of the diluting segment by the tubuloglomerular feedback mechanism and the ADH mechanism respectively. A new hypothesis on the pathogenesis of the water excretion inhibition in adrenal insufficiency is discussed.
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PMID:[On the etiology of water excretion inhibition in Addison's disease]. 726 45

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.
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PMID:[Supportive (antiinflammatory) treatment of bacterial meningoencephalitis with dexamethasone]. 937 71