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)

Sarcoplasmic reticulum (SR), Ca2+ plus Mg2+-ATPase, and Ca2+-ionophore were obtained from white rabbit skeletal muscles. Methylmercury inhibited the Ca2+ plus Mg2+-ATPase and Ca2+-transport but had no effect on the Ca2+-ionophore. Mercuric chloride inhibited all three functions (i.e., ATPase, transport and ionophoric activity). The mechanism of HgCl2 inhibition of the Ca2+-ionophore was by competition with Ca2+ for Ca2+-ionophoric site whereas its inhibition of the enzyme and Ca2+-transport was due to the blockage of essential sulfhydryl (--SH) groups. Ca2+ plus Mg2+-ATPase and Ca2+-transport were more sensitive to methylmercury than to HgCl2. Acetylcholine receptor (AChR) was obtained for the electric organ of T. californica. Methylmercury inhibited the ACh binding to AChR WITH Ki = 5.7 - 10(-6) M. This effect was not due to mercuric ion alone since mercuric chloride up to 10(-4) M did not affect ACh binding to AChR. It is concluded that: the Ca2+ plus Mg2+-ATPase and Ca2+-transport contain --SH groups essential for their activity, and that the two functions are tightly coupled; the Ca2+-ionophore contains no --SH groups essential for its activity; CH3HgCl inhibition of Ca2+ plus Mg2+-ATPase and Ca2+-transport is partly due to its reactivity with --SH groups in hydrophobic environment; the Ca2+-transport is inhibited by HgCl2 through two processes, one which is the blockage of --SH groups and another which is the inhibition of the Ca2+-ionophoric site; and the inhibition of ACh binding to AChR is due to the blockage of --SH groups in hydrophobic environment, which is inaccessible to Hg2+. Our data present for the first time a molecular basis for the myopathy associated with mercurial compounds toxicity.
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PMID:Differential effects of mercurial compounds on excitable tissues. 12 2

Under the effect of acetylcholine and vagal stimulation on the donor frog myocardium, a uridine polyphosphate-like substance (X-factor) is released. It intensifies contractions of the isolated heart-recipient and decreases the heart's sensitivity to acetylcholine and vagal stimulation. Acetylcholine (1-10(-4)-1-10(-5 g/ml) decreases UTPase activity (by 20-25%) and ATPase activity (by 15%) in isolated ventricle of the frog heart. When acetylcholine is washed away, UTPase activity is almost completely restored. Suppression of UTPase activity by acetylcholine seems to be one of the mechanisms responsible for the accumulation and release and uridine polyphosphates in the heart muscle.
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PMID:[Role of nucleoside triphosphatase in the formation of factor-X in frog myocardium following exposure to acetylcholine]. 14 28

In experiments in vitro at 37 and 17 degrees C, studies have been made of the effect of ACh upon the activity of Mg- and Na,K-ATPase of brain synaptosomes of the ground squirrel in summer animals and during winter hibernation. ACh (6 mM) decreases the activity of ATPases by 23-33% at 37 degrees C. During winter hibernation, the inhibitory effect of ACh is increased resulting in lower values of residual ATPase activity after the effect of ACh as compared with those obtained in summer period.
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PMID:[Action of acetylcholine on the adenosine triphosphatase activity of the brain synaptosomes of the suslik, Citellus erythrogenus]. 14 89

Synaptosomal fractions and synaptosomal membranes from rat brain tissue were prepared and characterized enzymatically. Arecoline increased both the activity of K+-phosphatase in incubated synaptosomal fractions and the (Na+ + K+)-ATPase activity of synaptosomal membranes by 40% and 78%, respectively. This activation of ion transport processes is believed to be associated with increased ACh synthesis produced by arecoline.
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PMID:Effect of arecoline on synaptosomal K+-phosphatase and (Na+ + K+)-ATPase. 18 59

1. After a local lesion of the diaphragm muscle, which produced a segment of innervated muscle fibres connected with an intact nerve-free segment by a region of crushed muscle fibres, the sensitivity to ACh, the presence of tetrodotoxin resistant action potentials (AP) and the transmission of AP along the muscle fibres were studied. 2. Three days after local injury of the diaphragm muscle ACh sensitivity and TTX resistance appeared in the crushed and nerve-free segments between the place of injury and the tendineous attachment. 5-7 days after injury transmission of action potentials through the damaged to the undamaged ("decentralized"), nerve-free part of the fibres is restored. High ACh sensitivity and TTX resistance of the latter segment, however, are completely lost only 20 days after the local injury. During this period contractility of the muscle remains practically unchanged. Enzymatic activities (SDH, ATPase and phosphorylase) of the damaged part were lost 3 days after crushing and recovered slowly between 7-10 days of regeneration of the diaphragm muscle fibres. 3. The experiments suggest that during regeneration of damaged muscle fibres supersensitivity to ACh remains high inspite of normal AP activity and that intracellular mechanisms may be involved in the induction and disappearance of ACh hypersensitivity.
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PMID:Control of ACh sensitivity in temporarily unconnected ("decentralized") segments of diaphragm-muscle fibres of the rat. 18 11

Acetylcholine (10(-6)--10(-3) M) added to the rat brain homogenate increased that activity of microsomal Na, K-ATPase and (14C)-amino acid incorporation in microsomal proteins. Actinomicin D (5.10(-5) M) eliminated the effect of acetylcholine. It is concluded that acetylcholine induced the synthesis of either Na, K-ATPase itself or some other proteins involved in the enzyme activity regulation.
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PMID:[Correlation of Na,K-ATPase activity and protein synthesis in nerve cell membranes exposed to acetylcholine]. 21 15

1. Acetylcholine (ACh) released from mouse diaphragm was gel filtrated and estimated by bio-assay and compared with electrophysiologically measured quantal release, expressed either as frequency of miniature end-plate potentials or quantum content of end-plate potentials. 2. Activation of Na+-K+-dependent membrane ATPase (membrane ATPase) in Na+-loaded muscles lowered the total amount of ACh released at rest to one tenth of the control value, but quantal release remained unchanged. 3. Inhibition of membrane ATPase by 2 X 10(-5) M-ouabain or by K-free solution led to an increase in total release and to a delayed progressive increase in quantal release. When Ca2+ was removed only the total release was enhanced. 4. Depolarization of the diaphragm by 8, 11 and 14 mM-K increased both total and quantal release only in the presence of Ca2+ in the perfusion medium. When Ca2+ was removed, no significant increase in release was observed. 5. The total and quantal release in response to 2 Hz stimulation of the preparation was increased 1.4 and 45 times, respectively. It is concluded that the total amount of ACh released at rest consists of two fractions, quantal and non-quantal, the former representing about 1% of the total release.
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PMID:Changes in total and quantal release of acetylcholine in the mouse diaphragm during activation and inhibition of membrane ATPase. 22 Apr 10

We investigated the effects of eserine and ouabain on the permeability of the blood-brain barrier (B.B.B.) as related to the febrile response induced with LPS in rabbit. Results are as follows; The febrile response induced by LPS (0.02 and 1.0 mug/kg) i.v. was suppressed by administration of ouabain (0.06 mg/kg, i.v.). Contrary to the febrile response of LPS given i.c. (10(-4) and 10(-3) mug/kg), the febrile response was not suppressed with the same dose of ouabain. The pyrogenicity of cerebrospinal fluid (CSF) withdrawn at two hours after rabbits had been injected with LPS (25 mug/kg) was suppressed by ouabain (0.06 mg/kg, i.v.). Pyrogenic response was enhanced by pretreatment with eserine (0.5 mg/kg, s.c.) given one hr before LPS (1 mug/kg, i.v.). The pyrogenicity of CSF was also potentiated to a greater extent by pretreatment of eserine than with LPS alone. In the eserinized rabbit (0.5 mg/kg, s.c.), the pyrogenicity of CSF was potentiated to a greater extent by ACh (10 mug/kg, i.v.) than by LPS (1 mug/kg, i.v.) alone. From these data, it is concluded that the inhibition of Na, K-ATPase by ouabain decreases the pyrogenicity of LPS, while the inhibition of cholinesterase by eserine enhances the pyrogenicity.
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PMID:[Effects of eserine and ouabain on the febrile reaction induced by lipopolysaccharide]. 103 14

Vesamicol is a highly potent inhibitor of active acetylcholine transport into isolated cholinergic vesicles from Torpedo. On the basis of transport kinetics and vesamicol sensitivity, we have shown that the acetylcholine transporter could be in an activated state even in the absence of a stimulated ATPase. In this preparation, N,N'-dicyclohexylcarbodiimide (DCCD), an hydrophobic carbodiimide, inactivates both ACh transport and vesamicol binding. Inhibition of vesamicol binding by DCCD is time dependent, saturable and prevented by vesamicol. DCCD first affected the affinity constant for vesamicol. Ki-value for DCCD lies in the micromolar range. These results imply that there is a DCCD reactive site within the ACh transporter and that it is located in an hydrophobic environment near the vesamicol binding site. SDS-gel electrophoresis after labelling of the vesicle membrane proteins with [14C]DCCD shows that radioactivity is mainly incorporated in a 15 kDa subunit. Time-course and concentration dependence of [14C]DCCD labelling and vesamicol inhibition do not coincide. Hence, the two processes are probably unrelated and the result rather points to another inactivation mechanism which can be an intramolecular cross link.
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PMID:Effect of N,N'-dicyclohexylcarbodiimide on the binding of vesamicol, an inhibitor of acetylcholine transport into synaptic vesicles. 130 45

The effect of Amiodarone (AD), a cationic amphiphilic drug, on erythrocytes and leucocytes was studied. Treatment of rats with AD showed a significant decrease in the red cell count and the level of Hemoglobin. Amiodarone altered the fluidity of the erythrocyte membrane followed by a decrease in the activities of membrane bound enzymes like (Na+, K+)-ATPase, Acetylcholine esterase and NADH dehydrogenase. A slight increase in the leucocyte count was also observed in the treated animals.
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PMID:Haematological and erythrocyte membrane changes induced by amiodarone, in rats. 133 99


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