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)

Two different procedures were employed for the isolation of sarcolemma from the rat heart and the membranes were studied with respect to the presence of cell surface material as well as their functional characteristics. Both hypotonic shock-LiBr treatment method (fraction HL) and sucrose density gradient method (fraction S) yielded membranes enriched 8 to 13 fold with respect to Na+-K+ ATPase and adenylate cyclase activities in comparison to heart homogenate. Cell surface material was demonstrated on the outer surface of the vesicles only in fraction HL with cationic dyes, lanthanum and ferritin, applied either to the isolated fractions or perfused in the heart through coronaries. Fraction HL also had high sialic acid content. ATP independent Ca2+ binding in fraction HL was about 6 times more than that in fraction S which had little sialic acid and showed no cell surface staining with cationic dyes. On the other hand, ATP-dependent Ca2+ binding and Ca2+-stimulated Mg2+ dependent ATPase activities in fraction S were 4 to 6 times higher than those in fraction HL. Epinephrine stimulated adenylate cyclase in fractions HL and S by 24 and 3% whereas ouabain was found to inhibit Na+-K+ ATPase in these fractions by 80 and 10% respectively. A mild treatment of the membranes with deoxycholate to eliminate the semipermeable characteristics or effects of sidedness of the vesicles resulted in an almost complete ouabain inhibition of Na+-K+ ATPase in both fractions. These data suggest that presence of cell surface material as well as membrane sidedness has an important role in in vitro expression of functional characteristics of sarcolemma. It is emphasized that sarcolemmal preparations containing cell surface material will provide information more realistic to the native conditions in situ.
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PMID:Differences in sarcolemmal preparations: cell surface material and membrane sidedness. 619 85

Adrenal chromaffin granules are known to possess an F1-ATPase which according to biochemical criteria is very similar to the mitochondrial one. To find a morphological equivalent for this enzyme chromaffin granules from bovine adrenal medullar were subjected to negative staining and freeze-etching. With both methods globular particles of 8 to 9 min diameter could be demonstrated on the surface of these organelles. A single granule possessed on average 22 particles. In negative staining the particles appeared separated from the membrane by a stalk of 8 nm. This typical morphological appearance was independent from a great variety of experimental procedures. After freeze-etching the particles were closely apposed to the membrane without any evidence for an interposed stalk. Pretreatment of chromaffin granules with pronase or trypsin led to a time dependent disappearance of the surface particles. In negative staining the stalked of chromaffin granules were found to be very similar in structure and size to those of mitochondria which have already been identified as F1-complexes. Based on this observation and other lines of evidence we suggest that the stalk particles found on the surface of chromaffin granules represent the F1-complex of the proton-pumping ATPase of these organelles.
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PMID:Adrenal chromaffin granules: evidence for an ultrastructural equivalent of the proton-pumping ATPase. 621 56

Noradrenaline (NA) sensitizes rat brain (Na+ + K+)-ATPase to inhibition by ethanol (EtOH). This effect of NA increases with the degree of enrichment of the enzyme: 0.1 mM NA + 0.05 M EtOH produced 27% inhibition in whole brain homogenates, 40% in 2.5-fold purified P2 fractions, and 45% in 5-fold purified microsomal fractions. The sensitization by NA was prevented by 0.1 microM phentolamine but not by 100 microM propranolol. Adrenaline and phenylephrine also sensitized the enzyme to EtOH inhibition in all of the fractions but isoproterenol did not. For all three alpha agonists the degree of sensitization was concentration dependent and the degree of reversal of this effect varied with the concentration of phentolamine added. These findings suggest that the NA + EtOH interaction is a direct effect on the membrane, probably mediated by an alpha receptor modified perturbation of the membrane microenvironment of the enzyme.
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PMID:Alpha adrenoreceptor mediated alteration of ethanol effects on (Na+ + K+)-ATPase of rat neuronal membranes. 626 Mar 17

Differences in the pattern of the development of three enzymes of the plasma membrane have been established. The activity of Na, K-ATPase progressively increases, that of adenylate cyclase decreases, whereas the activity of 5-nucleotidase undergoes only slight changes during embryogenesis. Differences between these enzymes were also found with respect to the development of their sensitivity to the regulatory effects of catecholamines. Adrenaline reactivity of adenylate cyclase may be detected already in embryogenesis; it is lower than that in definite muscle tissue increasing during further ontogenesis. Catecholamine reactivity was not found in Na, K-ATPase and 5-nucleotidase up to the 17th day of incubation of chick embryos. The effect of adrenalin was observed at later stages of ontogenesis, it may be initiated by exogeneous cAMP and protein kinase. At postembryonic stages, similarity in the behavior of these enzymes was found with respect to the presence and pattern of their reaction to adrenalin (stimulation), as well as with respect to temporal dynamics of the effect. The data obtained indicate the existence of close connections between these enzymes, which are realized in the sequence adrenoreceptor-adenylate cyclase-cAMP-protein kinase-effector proteins.
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PMID:[Role of the hypothalamus and pituitary gland in the development of pancreatic islet sensitivity to glucose in fetal rats]. 626 78

Sodium metavanadate (10(-4)-10(-6) M) stimulates the activity of adenylate cyclase and decreases the activity of Na+, K+-ATRase and 5'-nucleotidase in the sarcolemma fraction of chicken skeletal muscles at the embryonal and postembryonal developmental stages. Under conditions of a combined action of vanadate and guanylic nucleotides on the adenylate cyclase activity their effects are found to be potentiated. Epinephrine in vitro removes an inhibitory influence of vanadate on Na+, K+-ATPase from the third week of twe embryonal period. The restoring effect of epinephrine is blocked by propranol--a beta-adrenoblocker.
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PMID:[Effect of vanadium compounds on the enzymic activity in sarcolemma of developing muscles]. 628 70

Perfusion of pig jejunum with Escherichia coli heat-stable enterotoxin (strain 1261) reversed net absorption of water and electrolytes to net secretion. Addition of the alpha-adrenergic agonists clonidine (5 X 10(-7) M) or L-phenylephrine (5 X 10(-6) M), or the opiate agonist morphine (3.6 X 10(-6) M) to the perfusate reduced the secretory response to enterotoxin and stimulated absorption in normal jejunum. Epinephrine (5 X 10(-5) M) did not stimulate absorption in controls but reduced chloride loss in the presence of enterotoxin. Mucosal sodium--potassium adenosine triphosphatase was unchanged but disaccharidase activity was decreased in the presence of enterotoxin. The results suggest that alpha-adrenergic agonists and opiate agonists may exert an antidiarrheal action by increasing net transport across intestinal epithelium.
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PMID:Effects of epinephrine, clonidine, L-phenylephrine, and morphine on intestinal secretion mediated by Escherichia coli heat-stable enterotoxin in pig jejunum. 676 45

Adrenaline was infused intravenously in nine normal volunteers to plasma concentrations similar to those found after myocardial infarction. This study was undertaken on three occasions after 5 days' treatment with placebo or the beta-adrenoceptor antagonists, atenolol or timolol. Adrenaline increased the systolic pressure by 11 mmHg, decreased the diastolic pressure by 14 mmHg, and increased the heart rate by 7 beats/min. These changes were prevented by atenolol. However, after timolol the diastolic pressure rose (+19 mmHg) and heart rate fell (-8 beats/min). Adrenaline caused the corrected QT interval (QTc) to lengthen (0.36 +/- 0.02 s to 0.41 +/- 0.06 s). No significant changes were found in the QTc when subjects were pretreated with atenolol or timolol. The serum potassium fell from 4.06 to 3.22 mmol/l after adrenaline. Serum potassium fell to a lesser extent to 3.67 mmol/l after atenolol and actually increased to 4.25 mmol/l after timolol. Adrenaline-mediated hypokalaemia appears to result from the stimulation of a beta 2-adrenoceptor linked to membrane Na+/K+-ATPase causing potassium influx.
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PMID:The effects of cardioselective and non-selective beta-adrenoceptor blockade on the hypokalaemic and cardiovascular responses to adrenomedullary hormones in man. 686 46

The release studied by incubating tissue slices in an enriched, oxygenated medium in the presence and absence of secretagogues indicated that slices from 1-day-old rats released K+ in response to carbamylcholine, but not in response to epinephrine. The response to carbamylcholine was dose-related, with a 12.6 +/- 1.3 per cent release at a concentration of 2 X 10(-5) M. Epinephrine did not induce K+ release in concentrations from 2 X 10(-7) to 2 X 10(-4) M. Glands from 7- and 14-day-old rats released a similar amount as those of newborns in response to carbamylcholine and by 21 days of age the glands released 21.5 +/- 1.9 per cent of their K+ content upon exposure to 2 X 10(-5) M carbamylcholine. A response to epinephrine (2 X 10(-5) M) was first detected at 14 days of age, when the slices released 8.3 +/- 1.2 per cent of their K+. Slices of 21-day-old rats showed a 17.9 +/- 1.3 per cent K+ release in response to this dose. As in adult glands, the net amount of K+ released by the developing postnatal gland seems to be the result of two opposing mechanisms, a passive efflux and an active re-uptake which depends on the activation of an ouabain-sensitive Na+ -K+ -ATPase. The passive efflux component was similar in glands from different postnatal ages and was enhanced by secretagogues. The extent of active uptake, on the other hand, decreased with increasing postnatal age. As in the adult, the net release of K+ depended on the presence of Ca2+ in the incubation medium, but the sensitivity of the response to Ca2+ omission varied in accord with the age of the animals and with the stimulant used. It is speculated that proacinar and terminal tubular cells may be involved in K+ release in the early postnatal period.
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PMID:In-vitro release of K+ from the developing submandibular gland of early postnatal rats. 696 10

Gastric intubation of female Sprague-Dawley rats (80-150 g) with one large dose (5 g/kg) of ethanol nearly doubled oxygen uptake of the isolated, perfused rat liver in only 2.5 hours. This increased hepatic respiration can account for the Swift Increase in Alcohol Metabolism (SIAM). Inhibition of enhanced oxygen and ethanol uptake by KCN (2 mM) and 4-methylpyrazole (0.8 mM) indicated the involvement of the mitochondrial respiratory chain and alcohol dehydrogenase in this phenomenon, respectively. Epinephrine (2 mg/kg, i.p.) mimicked the increase in respiration observed with ethanol; however, the effects of epinephrine and ethanol were not additive. Pretreatment with alpha- and beta-adrenergic blocking agents, hypophysectomy and adrenalectomy prevented the increase in oxygen and ethanol uptake due to ethanol treatment. These data suggest that hormones including epinephrine are involved in the mechanism of SIAM. Hormone action in all likelihood activates a number of metabolic ATPase activities which lead to elevated oxygen uptake. One such process involved in the activation of oxygen uptake is diminished glycolysis, a ATP producing reaction sequence. The ADP not phosphorylated in the cytosol then enters the mitochondria where it stimulates oxygen uptake and NADH reoxidation. This ultimately leads to an acceleration of ADH-dependent ethanol metabolism.
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PMID:Mechanism of the swift increase in alcohol metabolism ("SIAM") in the rat. 742 36

Previously, we reported that the venom of Bufo marinus toad contains a Na+,K(+)-ATPase inhibitor with potent vasoconstrictor activity. In the present study, using thin-layer chromatography in Silicagel 60 F254 + 366, we separated a vasoactive substance from a mixture of steroids from Bufo marinus venom. Based on chromatographic mobility of this substance and typical color reaction after its vizualization with SbCl3, we identified it as a previously described steroid, marinobufagenin. Vasoconstrictor and Na+,K+ pump inhibitory properties of marinobufagenin were studied in isolated rat aortic rings and compared with those of ouabain. Ouabain (10-100 mumol.1-1) produced weak vasoconstriction, which was blocked by 2 mumol.1-1 phentolamine. 10 mumol.1-1 ouabain stimulated, and at higher concentrations inhibited, the Na+,K+ pump. 2 mumol.1-1 phentolamine abolished the activating effect of 10 mumol.1-1 ouabain on the Na+,K+ pump, but did not alter the inhibitory action of higher concentrations of ouabain. By contrast, marunibufagenin elicited rapid and strong vasoconstriction and inhibited ouabain-sensitive 86Rb uptake. Antidigoxin antibody antagonized the vasoconstrictor responses to marinobufagenin, but not to ouabain. 2 mumol.1-1 phentolamine did not alter the constrictor effect of marinobufagenin. In solid-phase digoxin immunoassay, marinobufagenin demonstrated higher digoxin-like immunoreactivity than ouabain.
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PMID:Effects of two endogenous Na+,K(+)-ATPase inhibitors, marinobufagenin and ouabain, on isolated rat aorta. 776 67


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