Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Na-K-ATPase has an important role in intestinal sodium and fluid absorption. We tested the colonic activity of this enzyme in patients with active ulcerative colitis to elucidate its role in the pathogenesis of the diarrhea associated with this disease. Colonic Na-K-ATPase activity in 13 patients with active ulcerative colitis prior to therapy was one-fourth of its activity in 14 normal subjects: 0.68 +/- 0.13 (SE) and 2.60 +/- 0.45 mumol/h . mg protein, respectively. In six patients with active ulcerative colitis on steroid therapy, the enzyme activity was similar to that observed in normal subjects. These results indicate an inhibition of colonic Na-K-ATPase activity in active ulcerative colitis, which may contribute to intestinal fluid accumulation and thus to the diarrhea in this disease.
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PMID:Decreased colonic Na-K-ATPase activity in active ulcerative colitis. 608 28

Assays for (Na+-K+)-ATPase and basal, fluoride stimulated and percentage of activation of adenylate cyclase have been established for small portions of human jejunal biopsies. Control means and ranges have been established for each activity in a group of children with failure to thrive but no gastrointestinal disease. Activities of (Na+-K+)-ATPase and percentage of activation and basal activity of adenylate cyclase are increased in children with toddler diarrhea. (Na+-K+)-ATPase activity is reduced in children with active postenteritis syndrome, and recovery from this syndrome is associated with an increase in this activity and of percentage of activation and basal activity of adenylate cyclase.
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PMID:Mucosal (Na+-K+)-ATPase and adenylate cyclase activities in children with toddler diarrhea and the postenteritis syndrome. 625 79

Twelve patients with recurrent polyserositis (RP, familial Mediterranean fever) on colchicine prophylaxis (1.0-2.0 mg daily) for three years or more were evaluated for the presence of gastrointestinal effects possibly attributable to the drug. Two patients had bulky stools, two others had transient diarrhea, and one had heartburn. Serum vitamin B12, calcium, and carotene levels were normal in all cases, and D-xylose absorption was normal in 11 of the 12. Three patients had mild steatorrhea (7.5, 7.9, and 9.9 g daily). Jejunal biopsies from these and a fourth patient with bulky stools but normal fecal fat excretion showed no abnormal histological changes. However, (Na + K)-ATPase activity was significantly decreased in all four cases. Colchicine had to be discontinued in only one of the 12 cases. It is concluded that mild steatorrhea and enzyme inhibition may occur in patients on long-term colchicine prophylaxis and that careful periodic observations for this and other adverse effects is imperative in such patients.
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PMID:Gastrointestinal effects of long-term colchicine therapy in patients with recurrent polyserositis (familial mediterranean fever). 628 60

The colon participates in water and electrolyte homeostasis by the absorption of sodium (Na) and water as well as by potassium (K) secretion. The primary step of colonic transport is the active Na transport via a transcellular route. Steroidal hormones considerably increase Na absorption by utilizing two mechanisms: (1) passive Na entry into the cells in enhanced by an increased membrane permeability; (2) active transport capacity is increased by a stimulation of ATPase synthesis. Mineralocorticoid versus glucocorticoid actions of steroids have not yet been clearly differentiated; parallel influences are possible. Active chloride (Cl) secretion is found in the colon under certain pathological conditions and is induced by a number of factors, e.g., hormones produced by pancreas tumors. Cellular events involve a rise of intracellular cAMP and calcium (Ca) concentrations, and altered Cl permeabilities. Functional changes of colonic epithelial cells caused by hormones assume a significant role in the etiology of diarrhea, as well as in compensatory processes by which an intestinal loss of electrolytes and water is prevented.
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PMID:Hormonal regulation of electrolyte and water transport in the colon. 638 47

Orally administered cadmium has been known to cause diarrhea and flatulence of the gastrointestinal tract. Scanning electron microscopic observations revealed that the absorptive cells on the tip of the intestinal villi were affected to some extent by administration of 2.5 microgram CdSO4/10 g of body weight (b. w.). Administration of higher doses of CdSO4 made the microvilli of the absorptive cells sparse and caused degeneration of the cells. Strong enzymic activities of alkaline phosphatase, acid phosphatase, magnesium-dependent ATPase, and sodium-potassium-dependent ATPase were recognized at the microvilli of the absorptive cells of the villi in the control mice. The enzymic activities of magnesium-dependent ATPase and sodium-potassium-dependent ATPase became weak with increasing dosages of CdSO4. The microvilli of the absorptive cells showed a strong alkaline phosphatase activity at a dose less than 25 microgram CdSO4/10 g of b. w., while some inhibitory effects could be recognized with 50 microgram/10 g of b. w. After administration of 2.5 microgram CdSO4/10 g of b. w., no acid phosphatase reaction products were found only at the absorptive cells located on the tip of the villi. Administration of a large quantity more than 5 microgram/10 g of b. w. strongly affected the acid phosphatase activity. It may be possible that the digestive functions are impaired by low cadmium administration.
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PMID:Scanning electron microscopic and enzyme histochemical observations on the cadmium-affected gastrointestinal villi of mice. 645 14

The pathogenesis of diarrhea caused by rotavirus infection was studied in miniature swine piglets. The animals were inoculated orally with 2 X 10(7) plaque-forming units of porcine rotavirus (OSU strain). During the height of diarrhea, intestinal function was investigated by in vivo perfusion of a 30-cm segment of proximal jejunum and a 30-cm segment of distal ileum. Absorption of Na+ and water decreased and 3-O-methylglucose transport was markedly reduced, P less than 0.01 compared to control animals. Mucosal lactase and sucrase levels were depressed in both the jejunum and ileum, P less than 0.001. Na+,K+-ATPase activity was significantly depressed only in the ileum, P less than 0.001. These changes were associated with a marked reduction in villous height, suggesting that the diarrhea could be an osmotic diarrhea due to nutrient (carbohydrate) malabsorption. Fresh stool samples were obtained and analyzed immediately for NA+,K+, osmolarity, glucose, and lactose; the osmotic gap was also determined. Stool osmolarity continually increased from 248 +/- 20 mosm/liter prior to inoculation to 348 +/- 20 mosm/liter at 75 +/- 1 hr postinoculation (P less than 0.005); the majority of the fecal osmotic gap could be accounted for by the amount of lactose present in the stools. Stool sodium increased from 34 +/- 6 mM prior to inoculation to a maximum of 65 +/- 4 mM at 53 +/- 1 hr postinoculation, P less than 0.001. There was no significant change in potassium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathogenesis of rotavirus-induced diarrhea. Preliminary studies in miniature swine piglet. 648 82

Intraluminal perfusion with Escherichia coli heat-stable enterotoxin (ST) reversed water and electrolyte movements from net absorption to net secretion in porcine jejunal segments. Addition of berberine hydrochloride (3.2 X 10(-5) M) to the perfusate reduced the jejunal secretory response of water, sodium, potassium, and chloride to ST and enhanced water and electrolyte absorption in control segments. At lower concentrations (1.1 X 10(-5) M), berberine reduced the secretory response in ST-exposed segments, but only the decrease of sodium flux was significant. In the presence of berberine, the mucosal enzyme activities of adenosine triphosphatase and disaccharidases were not significantly different between control and ST-exposed segments. Doses of 1, 2, 3, 4, 5, and 10 mg of berberine were injected into ligated loops of proximal part of the jejunum with 1 ml of ST filtrate. At doses of 2 or more mg/loop, berberine was effective in reducing water and electrolyte secretions induced by ST; the effect was dose-dependent. These findings indicate that berberine may be an effective antidiarrheal agent in E coli heat-stable enterotoxin mediated secretory diarrhea and provide a basis for the frequent empirical use of berberine alkaloid and berberine-containing plants in gastroenteritis and infectious diarrhea in Asian and other countries.
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PMID:Effect of berberine on intestinal secretion mediated by Escherichia coli heat-stable enterotoxin in jejunum of pigs. 675 29

Intraluminal perfusion of pig jejunum with Escherichia coli heat-stable enterotoxin reversed net absorption of water and electrolytes to net secretion. Addition of atropine (2 x 10(-5)M) to the perfusate reduced the secretory response to enterotoxin and enhanced sodium and chloride absorption in control segments. Indomethacin (1.4 x 10(-3)M), acetazolamide (2.2 x 10(-3)M), or ethacrynate sodium (3.1 x 10(-4)M) had no effect. Mucosal disaccharidase activity and Na-K-ATPase activity were not altered by enterotoxin. The results suggest that blockade of cholinergically mediated secretion in the small intestine attenuates the enterosorptive effects of heat-stable enterotoxin and may be useful therapeutically in the management of secretory diarrhea.
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PMID:Effects of indomethacin, acetazolamide, ethacrynate sodium, and atropine on intestinal secretion mediated by Escherichia coli heat-stable enterotoxin in pig jejunum. 675 23

Unless renal function is impaired or rhabdomyolysis is severe, hyperkalemia is a relatively uncommon metabolic complication of poisoning. In contrast, marked hypokalemia is a more common problem and may have serious sequelae. Most potassium disturbances in acute poisoning are due to disruption of extra-renal control mechanisms, notably the activity of Na+/K+ ATPase and K+ channels. Hypokalemia occurs because of increased Na+/K+ ATPase activity (e.g. beta 2 agonist, theophylline or insulin poisoning), competitive blockade of K+ channels (e.g. barium or chloroquine poisoning), gastrointestinal losses and/or alkalosis. Hyperkalemia follows inhibition of Na+/K+ ATPase activity (e.g. by digoxin), increased uptake of potassium salts, disruption of intermediary metabolism (e.g. cyanide poisoning), activation of K+ channels (e.g. fluoride poisoning), and the presence of acidosis and rhabdomyolysis, particularly if the latter is complicated by renal failure. Hypokalemia results in generalized muscle weakness, paralytic ileus, ECG changes (flat or inverted T waves, prominent U waves, ST segment depression) and cardiac arrhythmias (atrial tachycardia +/- block, AV dissociation, VT, VF). Hyperkalemia is associated with abdominal pain, diarrhea, muscle pain and weakness, ECG changes (tall peaked T waves, ST segment depression, prolonged PR interval, QRS prolongation) and cardiac arrhythmias (VT, VF). Significant disturbances of potassium homeostasis are often unrecognized and may cause considerable morbidity and mortality. Prompt recognition and appropriate treatment of these disturbances could be life-saving.
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PMID:Disturbances of potassium homeostasis in poisoning. 762 96

Clinical manifestations of leptospirosis include disorders of the electrolytical balance which might be related to inhibition of Na,K-ATPase. Although the physiopathological cellular mechanism of leptospirosis remains unknown, a bacterial endotoxin has been incriminated. Therefore, we evaluated whether a glycolipoprotein fraction extracted from Leptospira interrogans and known to be cytotoxic might inhibit Na,K-ATPase. This glycolipoprotein fraction (GLP) inhibited Na,K-ATPase activity in rabbit kidney epithelial cells as well as Na,K-ATPase purified from rabbit kidney medulla. Inhibition was dose-dependent, and at maximum it almost abolished Na,K-ATPase activity whereas it had no effect on other enzymes. The GLP did not change the apparent affinity of Na,K-ATPase for potassium whereas it increased that for sodium, revealing a mechanism of inhibition different from that of ouabain. Finally, the inhibitory principle present in the GLP preparation was thermostable and was curtailed by the presence of albumin. In conclusion, a glycolipoproteic fraction extracted from Leptospira interrogans contains a specific inhibitor of Na,K-ATPase. This glycolipoproteic fraction which is present in diseased tissues might induce, through this inhibitor, cellular dysfunctions responsible for the symptoms, in particular those associated with electrolytical disorders such as disturbances of renal electrolyte handling, cardiac arrhythmia or diarrhoea.
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PMID:Inhibition of Na,K-ATPase by an endotoxin extracted from Leptospira interrogans: a possible mechanism for the physiopathology of leptospirosis. 767 Oct 8


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