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)

Rats were subjected to hypokinesia for two months and the contractile function of isolated papillary muscles was studied. Hypokinesia reduced significantly the isotonic contraction velocity which depended on the ATPase activity of the myofibrils; it also reduced the velocity and index of relaxation which depended on the functional capacity of the Ca++-pump of the sarcoplasmic reticulum. The maximum force of isometric contraction determined by the quantity of actomyosine bridges in the myofibrils did not change after hypokinesia. This complex of changes is contrary to that observed in adaptation to exercise, when the velocity of isotonic contraction and relaxation increases while the force of isometric contraction does not change. The possible mechanism of this stability of the contractile force during adaptation and readaptation of the heart is discussed.
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PMID:[Effect of hypokinesia on the contractile function of the myocardium]. 42 40

Plasmin activity in the tear fluid of the rabbit eye was examined during the wearing of soft contact lenses (SCL) and compared with the occurrence of corneal disturbances assessed in cryostat sections. Plasmin activity was determined with a semiquantitative method using dry punches of filter paper previously soaked in 0.1 M Tris-HCl buffer solution containing mmol/l D-Val-Leu-Lys-FCA (trifluoromethylaminocoumarine), pH 7.2. Punches were applied to the corneal surface for 5 s (tear collection) and incubated in wet chamber. The time of appearance of the bright yellow fluorescence in UV light was recorded and taken as a measure of plasmin activity. For calibration punches soaked in solutions containing plasmin in various concentrations, and processed in the same manner were used. Changes in the cornea were examined histochemically using methods of choice for acid glycosidases, proteases, dehydrogenases, and Na(+)-K(+)-ATPase. SCL with high and low water content were worn in rabbits in 1, 2, 4, 7, 14, 21 and 28 days. Decreased activity of Na(+)-K(+)-ATPase, GGT, and SDH in the corneal endothelium and epithelium were not accompanied by detectable plasmin activity in the tear fluid. Pronounced damage of the corneal epithelium (increased activities of acid glycosidases, acid proteases, LDH, markedly decreased activity of SDH) was accompanied by low concentration of plasmin (0.4-1.0 micrograms/ml) in the tear fluid. Middle activity of plasmin (1.0-2.0 micrograms/ml) was detectable when PMNs were present in the corneal stroma. High plasmin activity (2.0-3.0 micrograms/ml) correlated with corneal ulceration and vascularization.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histochemical changes in the rabbit cornea and plasmin activity in the tear fluid during contact lens wear. Favourable influence of protease inhibitors (aprotinin, PC5, elastatinal). 137 62

In 10 southern Indian patients with tropical sprue, in vivo dialysis showed a defect of absorption of water and sodium from the rectum, when compared with 11 healthy volunteers. Sodium-potassium-ATPase activity, measured in homogenates of rectal biopsies, was significantly diminished in patients with sprue. Magnesium-ATPase and alkaline phosphatase were normal in biopsy homogenates. Decreased activity of colonic sodium-potassium-ATPase may contribute to diarrhoea in some patients with tropical sprue.
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PMID:Absorption of water and sodium and activity of adenosine triphosphatases in the rectal mucosa in tropical sprue. 284 Mar 63

We have previously shown that red blood cell (RBC) filtrability in uncontrolled insulin dependent diabetics is abnormal compared to healthy subjects, but is corrected by insulin added in vivo or in vitro. We have now found biophysical abnormalities of the RBC membrane in such patients: Fluorescence polarization value (p) evaluated using DPH as probe is significantly lower in patients; insulin added in vitro increases and normalises the p value of diabetic RBC membrane, and has no effect on normal RBC membrane. As there is a relationship between the lipid bilayer and membrane cytoskeleton proteins, this abnormality of RBC membrane fluidity, correctable by insulin, may be an important determinant of the rheological behaviour of the RBC. In parallel, biochemical abnormalities of the RBC membrane are shown in the same patients: Higher cholesterol/phospholipid ratio, lower content in unsaturated fatty acids and higher content in saturated fatty acids. Decreased activity of ouabaine sensitive Na+K+ ATPase and increased activity of Mg++ ATPase. All of these RBC biochemical abnormalities are corrected after 24 h of normoglycaemia obtained by insulin treatment given in vivo with a biostator. Our results show the importance to check the degree of control of glycaemia when studying rheological parameters in diabetes mellitus.
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PMID:Rapid modifications of biophysical and biochemical parameters of red blood cell membrane from insulin dependent diabetics after insulin administration. 302 39

We studied changes in hepatic membrane (Na+,K+)ATPase activity and membrane lipids induced by canrenoate, the water-soluble congener of canrenone, the active metabolite of spironolactone. (Na+,K+)ATPase activity was decreased after canrenoate in a dose- and time-dependent manner. Decreased activity was demonstrated at the lowest dose (91% of control after 5 mumoles per 100 gm body weight per day X 3 days); the maximum dose (30 mumoles per 100 gm body weight per day X 3 days) resulted in activity 38% of untreated control values. A 20 mumoles per 100 gm body weight per day dose decreased enzyme activity to 89 and 55% of control after 24 and 72 hr, respectively. The nonionic detergent Triton WR-1339 partially reversed drug-induced inhibition, suggesting that the enzyme changes may be related to altered membrane lipids. Membrane cholesterol increased 17% after 3 days of 30 mumoles canrenoate per 100 gm body weight per day; phospholipids decreased by 12%. The cholesterol to phospholipid molar ratio increased from 0.419 to 0.555. Membrane fluidity, as measured by the fluorescent probe 1,6-diphenyl-1,3,5-hexatriene decreased after treatment with 20 mumoles canrenoate per 100 gm body weight per day for 3 days. These results describe in vivo and in vitro inhibition of hepatic (Na+,K+)ATPase activity. Increased membrane cholesterol with decreased phospholipid alters membrane fluidity and may be partially responsible for the change in (Na+,K+)ATPase activity.
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PMID:Spironolactone- and canrenone-induced changes in hepatic (Na+,K+)ATPase activity, surface membrane cholesterol and phospholipid, and fluorescence polarization in the rat. 630 16

The effect of DL alpha-lipoic acid on the nephrotoxic potential of gentamicin was examined. Intraperitoneal injection of gentamicin (100 mg/kg/day) to rats resulted in decreased activity of the glycolytic enzymes-hexokinase, phosphoglucoisomerase, aldolase and lactate dehydrogenase. The two gluconeogenic enzymes--glucose-6-phosphatase and fructose-1,6-diphosphatase, the transmembrane enzymes namely the Na+, K(+)-ATPase, Ca(2+)-ATPase, Mg(2+)-ATPase and the brushborder enzyme alkaline phosphatase, also showed decreased activities. This decrease in the activities of ATPases and alkaline phosphatase suggests basolateral and brush border membrane damage. Decreased activity of the TCA cycle enzymes isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH) and malate dehydrogenase (MDH), suggests a loss in mitochondrial integrity. These biochemical disturbances were effectively counteracted by lipoic acid administration. Lipoic acid administration by gastric intubation at two different concentrations (10 mg and 25 mg/kg/day) brought about an increase in the activity of the glycolytic enzymes, ATPases and the TCA cycle enzymes. The gluconeogenic enzymes however showed a further decrease in their activities at both the concentrations of lipoic acid administered. These observations shed light on the nephroprotective action of lipoic acid against experimental aminoglycoside toxicity and the protection afforded at 25 mg/kg/day of lipoic acid was noted to be higher than that at 10 mg level.
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PMID:Role of DL alpha-lipoic acid in gentamicin induced nephrotoxicity. 765 73

Normal auditory function depends on the maintenance of the unique ion composition in the endolymph. The Na(+)-K(+)-ATPase in the lateral wall of the cochlear duct has been suggested to play an important role in maintaining the endolymphatic ion concentration and in generating a positive endocochlear potential. Cochlear dysfunction may indicate changes in the biochemical components and osmotic pressure of the inner ear fluids as well as inadequate generation of intracellular metabolic energy. Dysfunction of the stria vascularis and spiral prominence was investigated in the early stages of endolymphatic hydrops. Vibratome sections of hydropic and normal cochleae were stained histochemically for Na(+)-K(+)-ATPase activity in this study. Decreased activity of this enzyme was shown in the stria vascularis and spiral prominence of the hydropic cochlea in the early stage of endolymphatic hydrops. The results coincide with those of studies of electrophysiologic changes in cochlear function in hydropic animals by others. The results of the present study provide further information concerning a possible deficit in ion transport activity and decreased enzymatic activity in the cochlea.
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PMID:Reduced Na(+)-K(+)-ATPase activities in the cochleae of guinea pigs with experimental endolymphatic hydrops. 810 45

The aim of this short review was to collate the data involving the effects of lithium alone, or in combination, with antidepressant drugs in several animal models of depression. It has been shown that lithium administration reduced immobility in the mouse forced swimming test when given 30 min, but not 45 min, before testing. Further studies indicated that this activity was probably a result of an activity on serotonin (5-HT) 1A and 1B receptor subtypes. Lithium treatment has been shown to reverse helpless behaviour in the learned helplessness model of depression after chronic treatment (30 days), where lithium was administered in the drinking water. Further studies showed that acute (5 days) administration of lithium failed to reverse behavioural deficits. In the olfactory bulbectomised rat model of depression, several immunological and enzymatic functions have been shown to be altered and these changes are regularised by antidepressant treatment as well as lithium administration for 15 days. Hypokinesia (reduced locomotor activity) is a phenomenon observed following immobilisation stress in rats. This behavioural deficit was attenuated by lithium together with a wide range of antidepressant drugs used in the treatment of unipolar depression at non-stimulant doses. In addition, a single administration of lithium slightly inhibited midbrain raphe lesion-induced muricidal behaviour (25%); however, repeated treatment (5 days) significantly attenuated this behavioural deficit. Lithium treatment has also been shown to reverse behavioural and biochemical deficits induced by reserpine together with those induced by acute administration of single intracerebroventricular (i.c.v.) dose of the Na, K-ATPase-inhibiting compound, ouabain. Long-term studies of lithium augmentation have not been performed, so that no clear recommendations for the duration of this therapy can be made. The points raised in this short review endorse the commencement of such studies.
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PMID:The effect of lithium administration in animal models of depression: a short review. 1039 5

Abnormalities in calcium flux have been linked to abnormal contractile behavior of the heart in patients with congestive heart failure as well as in animal models. Decreased activity or levels of the calcium adenosine triphosphatase of the sarco(endo)plasmic reticulum (SERCA2) particularly have been known to cause a delay in calcium transients. The SERCA2 protein pumps 2 moles of calcium per mole of adenosine triphosphate (ATP) split from the cytoplasm into the sarcoplasmic reticulum, thus lowering the free cytoplasmic calcium concentration. It therefore is of interest to identify mechanisms by which SERCA activity could be increased in the heart. To determine influences of increased expression of the SERCA2 gene on calcium transient and contractile behavior, we constructed transgenic mice and rats expressing a SERCA2 transgene in their heart. In these animals, a 20% increase in SERCA levels occurs due to additional expression of the SERCA transgene. This leads to a corresponding increase in contractile activity as determined by the increase in left ventricular pressure measured as dP/dt(max) and decrease in diastolic ventricular pressure determined as dP/dt(min). Similarly, isolated cardiac myocytes obtained from the heart of transgenic mice showed an accelerated calcium transient and increased speed of shortening and relengthening as determined by edge detection. To determine if SERCA2 transgene expression could have a compensatory effect on the contractile behavior of the heart in transgenic mice expressing SERCA2, these mice were made hypothyroid, and papillary muscle function was determined. Contractile behavior of the papillary muscle of wild-type hypothyroid mice showed a significant increase in muscle relaxation time (RT50). In contrast, SERCA2 transgenic hypothyroid mice showed normal contractile behavior of papillary muscle. A compensatory effect of SERCA transgene expression was therefore demonstrated. In addition, we constructed transgenic rats expressing a SERCA2 transgene in which constriction of the ascending aorta induced cardiac hypertrophy and a delayed contraction of papillary muscle. In preliminary results, we found that SERCA2 transgenic rats submitted to ascending aortic constriction did not show the delayed relaxation of papillary muscle as was found in wild-type rats submitted to aortic constriction. In addition, adenoviral vectors expressing transgenes for calcium-handling proteins can be used to improve cardiac myocyte contraction. Adenoviruses expressing a SERCA transgene or a mutant phospholamban transgene exhibiting dominant negative action were used to infect isolated myocytes treated with a phorbol ester (phorbol 12-myristate 13-acetate), which delays the calcium transients. The calcium transients and contractile behavior of the isolated myocytes indicated that increased SERCA expression or increased expression of mutant phospholamban transgene led to increased SERCA2 activity, resulting in an increased contractile phenotype. Recent findings by other investigators also indicate that decreased SERCA2 activity can be increased under in vivo conditions using adenoviral vector-based SERCA2 expression. A gene therapy type of approach delivering increased amounts of SERCA or phospholamban mutants leading to increased SERCA activity should therefore be considered in the future.
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PMID:Calcium regulatory proteins and their alteration by transgenic approaches. 1075 May 95

Transepithelial sodium transport via alveolar epithelial Na(+) channels and Na(+),K(+)-ATPase constitutes the driving force for removal of alveolar oedema fluid. Decreased activity of the amiloride-sensitive epithelial Na(+) channel (ENaC) in the apical membrane of alveolar epithelial cells impairs sodium-driven alveolar fluid clearance (AFC) and predisposes to pulmonary oedema. We hypothesized that hyperactivity of ENaC in the distal lung could improve AFC and facilitate the resolution of pulmonary oedema. AFC and lung fluid balance were studied at baseline and under conditions of hydrostatic pulmonary oedema in the beta-Liddle (L) mouse strain harbouring a gain-of-function mutation (R(566)(stop)) within the Scnn1b gene. As compared with wild-type (+/+), baseline AFC was increased by 2- and 3-fold in heterozygous (+/L) and homozygous mutated (L/L) mice, respectively, mainly due to increased amiloride-sensitive AFC. The beta(2)-agonist terbutaline stimulated AFC in +/+ and +/L mice, but not in L/L mice. Acute volume overload induced by saline infusion (40% of body weight over 2 h) significantly increased extravascular (i.e. interstitial and alveolar) lung water as assessed by the bloodless wet-to-dry lung weight ratio in +/+ and L/L mice, as compared with baseline. However, the increase was significantly larger in +/+ than in L/L groups (P=0.01). Volume overload also increased the volume of the alveolar epithelial lining fluid in +/+ mice, indicating the presence of alveolar oedema, but not in L/L mice. Cardiac function as evaluated by echocardiography was comparable in both groups. These data show that constitutive ENaC activation improved sodium-driven AFC in the mouse lung, and attenuated the severity of hydrostatic pulmonary oedema.
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PMID:beta-Liddle mutation of the epithelial sodium channel increases alveolar fluid clearance and reduces the severity of hydrostatic pulmonary oedema in mice. 1743 Sep 90


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