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)

The syndrome of inappropriate secretion of antidiuretic hormone was observed in two patients with cystic fibrosis during acute exacerbation of chronic pulmonary disease. It was diagnosed by the accepted clinical and laboratory criteria and confirmed in one case by values for immunoreactive vasopressin that were inappropriately high for plasma osmolality. The severe hyponatremia was corrected by fluid restriction, alone or combined with intravenous treatment with diuretic and hypertonic saline solution. In addition, there was simultaneous therapy of the pulmonary disease. SIADH thus must be added to salt loss as a cause of hyponatremia in CF, and may be more common than realized in patients with CF and severe pulmonary disease.
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PMID:The syndrome of inappropriate antidiuretic hormone secretion as a cause of hyponatremia in cystic fibrosis. 83 69

Desmopressin and vasopressin were used to control massive haemoptysis in a patient with cystic fibrosis. After bolus doses a continuous infusion of vasopressin was maintained for 36 hours and haemoptysis stopped.
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PMID:Life threatening haemoptysis in cystic fibrosis: an alternative therapeutic approach. 203 39

The amiloride-sensitive epithelial sodium channel (ENaC) contributes to the regulation of the sodium balance and blood pressure because it mediates a rate-limiting step in sodium transport across the epithelium of the distal nephron. The activity of ENaC is regulated by hormones, such as aldosterone and vasopressin, and by other intracellular or extracellular factors, but the mechanisms of these regulations are not yet well understood. It has been proposed that ENaC may be regulated by an associated ATP-binding cassette protein such as the cystic fibrosis conductance regulator or the K channel-associated sulfonylurea receptor. Glibenclamide, a known inhibitor of sulfonylurea receptor and cystic fibrosis conductance regulator, induced a dose-dependent and reversible stimulation (of the order of 40-50%) of the amiloride-sensitive current in oocytes expressing Xenopus ENaC, with a K1/2 of 45 +/- 5 microM. A similar effect was observed in oocytes expressing human ENaC, but not rat ENaC. Measurements performed with various combinations of rat and Xenopus subunits indicated that several subunits are involved in this effect. Glibenclamide also increased the transepithelial Na transport by the A6 Xenopus kidney cell line. Single-channel current recordings showed a doubling of the number of the open channels when glibenclamide was applied locally to the extracellular surface of the cell membrane. These results support the hypothesis of the existence of an associated ATP-binding cassette-type regulatory protein associated with the epithelial sodium channel.
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PMID:Stimulation of epithelial sodium channel activity by the sulfonylurea glibenclamide. 1038 97

The epithelial Na+ channel (ENaC) forms the pathway for Na+ absorption in the kidney collecting duct and other epithelia. Dominant gain-of-function mutations cause Liddle's syndrome, an inherited form of hypertension resulting from excessive renal Na+ absorption. Conversely, loss-of-function mutations cause pseudohypoaldosteronism type I, a disorder of salt wasting and hypotension. Thus, ENaC has a critical role in the maintenance of Na+ homeostasis and blood pressure control. Altered Na+ absorption in the lung may also contribute to the pathogenesis of cystic fibrosis. Epithelial Na+ absorption is regulated in large part by mechanisms that control the expression of ENaC at the cell surface. Nedd4, a ubiquitin protein ligase, binds to ENaC and targets the channel for endocytosis and degradation. Liddle's syndrome mutations disrupt the interaction between ENaC and Nedd4, resulting in an increase in the number of ENaC channels at the cell surface. Aldosterone and vasopressin also regulate Na+ absorption to defend against hypotension and hypovolemia. Both hormones increase the expression of ENaC at the cell surface. The goal of this review is to summarize recent data on the regulation of ENaC expression at the cell surface.
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PMID:The epithelial Na+ channel: cell surface insertion and retrieval in Na+ homeostasis and hypertension. 1194 47

The amiloride-sensitive epithelial sodium channel (ENaC), a multimeric plasma membrane protein composed of alpha-, beta-, and gamma-ENaC subunits, mediates Na(+) reabsorption in epithelial tissues, including the distal nephron, colon, lung, and secretory glands, and plays a critical role in pathophysiology of essential hypertension and cystic fibrosis (CF). The function of ENaC is tightly regulated by signals elicited by aldosterone, vasopressin, agents that increase intracellular cAMP levels, ions, ion channels, G-protein-coupled mechanisms, and cytoskeletal proteins. In this paper, the effects of Ca(2+) on the expression of the human ENaC subunits expressed in human embryonic kidney cells (HEK-293 cells) were examined. Incubation of cells with increased extracellular Ca(2+) and treatment of cells with A23187 and thapsigargin stimulated the expression of the monomeric ENaC subunits. Treatment of cells with Ca(2+)-chelating agents, EGTA and BAPTA-AM, reduced the levels of ENaC subunit expression. The pulse-chase experiments suggested that a rise in the intracellular Ca(2+) increases the ENaC subunit expression. Immunoblot analysis using the anti-ubiquitin antibody indicated that ENaC undergoes ubiquitination. A correlation between the processes that regulate ENaC function with the intracellular Ca(2+) was discussed.
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PMID:Role of intracellular Ca2+ in the expression of the amiloride-sensitive epithelial sodium channel. 1467 Mar 68

One of the major advances in modern medicine was the development of antimicrobial chemotherapy. However, many antibacterial agents have unexpected or undesirable nonantimicrobial effects on humans. Microbes and man share many essentials of life, including DNA, adenosine triphosphate, and other biochemical pathways. Hence, some of these nonantimicrobial effects may also turn out to be pharmacologically useful. Oral hypoglycemic agents (i.e., sulfonylureas) and a certain diuretic agent (acetazolamide) are derivatives of sulfonamides. Erythromycin has been used clinically for its stimulatory effect on gastrointestinal motility. Macrolides, lincosamides, and tetracyclines have been known for their immunomodulatory effects. A tetracycline has been used to treat the syndrome of inappropriate antidiuretic hormone. Aminoglycosides may influence mucus production in patients with cystic fibrosis. Other antimicrobials may have side effects that are not therapeutically useful, such as osmotic diuresis with high-dose beta -lactam administration, neuromuscular blockade of aminoglycosides, dysglycemia of fluoroquinolones, and serotonin syndrome with oxazolidinones.
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PMID:Nonantimicrobial effects of antibacterial agents. 1561 2

The epithelial Na(+) channel (ENaC) is a pathway for Na(+) transport across epithelia, including the kidney collecting duct, lung, and distal colon. ENaC is critical for Na(+) homeostasis and blood pressure control; defects in ENaC function and regulation are responsible for inherited forms of hypertension and hypotension and may contribute to the pathogenesis of cystic fibrosis and other lung diseases. An emerging theme is that epithelial Na(+) transport is regulated in large part through trafficking mechanisms that control ENaC expression at the cell surface. ENaC trafficking is regulated at multiple steps. Delivery of channels to the cell surface is regulated by aldosterone (and corticosteroids) and vasopressin, which increase ENaC synthesis and exocytosis, respectively. Conversely, endocytosis and degradation is controlled by a sequence located in the C terminus of alpha, beta, and gammaENaC (PPPXYXXL). This sequence functions as an endocytosis motif and as a binding site for Nedd4-2, an E3 ubiquitin protein ligase that targets ENaC for degradation. Mutations that delete or disrupt this motif cause accumulation of channels at the cell surface, resulting in Liddle's syndrome, an inherited form of hypertension. Nedd4-2 is a central convergence point for ENaC regulation by aldosterone and vasopressin; both induce phosphorylation of a common set of three Nedd4-2 residues, which blocks Nedd4-2 binding to ENaC. Thus, aldosterone and vasopressin regulate epithelial Na(+) transport in part by altering ENaC trafficking to and from the cell surface.
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PMID:Minireview: regulation of epithelial Na+ channel trafficking. 1615 Aug 99

DDAVP is a drug that should be used with caution for each patient individually. Particular care is needed to avoid fluid overload and rapid fluctuations in sodium concentration. Not only families but physicians as well should be educated and aware of the adverse effects of DDAVP, especially in high risk patients. Extreme caution is needed in children with severe neurological and developmental problems who cannot control their fluid intake themselves. Similarly, caution is needed in patients with hypodipsia and DI who have difficulty in balancing water intake and DDAVP dose. The treatment of DI is water; however, DDAVP is given to avoid a large fluid intake which can result in medullary washout. Frequent home monitoring of body weight and regular determinations of serum sodium may help to disclose the early phase of over-hydration or dehydration. DDAVP therapy should be temporarily interrupted during acute illness, febrile episodes, hot days and other conditions with increased water intake. It should be used with considerable caution in patients with cystic fibrosis, or renal or cardiovascular diseases. In patients with enuresis, it is recommended that DDAVP medication should not be continued for longer than 3 months without stopping for 1 week for full reassessment. Fluid intake should be limited 1 hour before and 8 hours after the dose. Generally, undertreatment with vasopressin analogue is safer than overtreatment. A simple measure to avoid overtreatment is to miss one dose once a week; a rapid onset diuresis ('washout' effect) provides considerable reassurance.
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PMID:Morbidity and mortality associated with vasopressin analogue treatment. 1660 17

Polycystic kidney diseases (autosomal dominant and autosomal recessive) are progressive renal tubular cystic diseases, which are characterised by cyst expansion and loss of normal kidney structure and function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common life- threatening, hereditary disease. ADPKD is more prevalent than Huntington's disease, haemophilia, sickle cell disease, cystic fibrosis, myotonic dystrophy and Down's syndrome combined. Early diagnosis and treatment of hypertension with inhibitors of the renin-angiotensin-aldosterone system (RAAS) and its potential protective effect on left ventricular hypertrophy has been one of the major therapeutic goals to decrease cardiac complications and contribute to improved prognosis of the disease. Advances in the understanding of the genetics, molecular biology and pathophysiology of the disease are likely to facilitate the improvement of treatments for these diseases. Developments in describing the role of intracellular calcium ([Ca(2+)](i)) and its correlation with cellular signalling systems, Ras/Raf/mitogen extracellular kinase (MEK)/extracellular signal-regulated protein kinase (ERK), and interaction of these pathways with cyclic adenosine monophosphate (cAMP) levels, provide new insights on treatment strategies. Blocking the vasopressin V(2) receptor, a major adenylyl cyclase agonist, demonstrated significant improvements in inhibiting cytogenesis in animal models. Because of activation of the mammalian target of rapamycin (mTOR) pathway, the use of sirolimus (rapamycin) an mTOR inhibitor, markedly reduced cyst formation and decreased polycystic kidney size in several animal models. Caspase inhibitors have been shown to decrease cytogenesis and renal failure in rats with cystic disease. Cystic fluid secretion results in cyst enlargement and somatostatin analogues have been shown to decrease renal cyst progression in patients with ADPKD. The safety and efficacy of these classes of drugs provide potential interventions for experimental and clinical trials.
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PMID:Potential pharmacological interventions in polycystic kidney disease. 1803 88

The epithelial Na(+) channel (ENaC) is a major regulator of salt and water reabsorption in a number of epithelial tissues. Abnormalities in ENaC function have been directly linked to several human disease states including Liddle's syndrome, psuedohypoaldosteronism, and cystic fibrosis and may be implicated in states as diverse as salt-sensitive hypertension, nephrosis, and pulmonary edema. ENaC activity in epithelial cells is highly regulated both by open probability and number of channels. Open probability is regulated by a number of factors, including proteolytic processing, while ENaC number is regulated by cellular trafficking. This review discusses current understanding of apical membrane delivery, cell surface stability, endocytosis, retrieval, and recycling of ENaC and the molecular partners that have so far been shown to participate in these processes. We review known sites and mechanisms of hormonal regulation of trafficking by aldosterone, vasopressin, and insulin. While many details of the regulation of ENaC trafficking remain to be elucidated, knowledge of these mechanisms may provide further insights into ENaC activity in normal and disease states.
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PMID:Regulation of the epithelial sodium channel by membrane trafficking. 1850 77


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