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Registros recuperados: 10 | |
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Fujikawa, Ryu; Muroi, Yoshikage; Unno, Toshihiro; Ishii, Toshiaki; 室井, 喜景; 石井, 利明. |
Botulinum neurotoxin serotype A (BoNT/A) inhibits acetylcholine release at the neuromuscular junction in isolated muscles, and ouabain can partially block its effect. However, it is not clear whether ouabain attenuates BoNT/A-induced neuromuscular paralysis in vivo. In this work, we investigated the effects of ouabain on BoNT/A-induced neuromuscular paralysis in mice. Ouabain was administered to mice intraperitoneally immediately after a single injection of BoNT/A into skeletal muscle. The effects of ouabain on BoNT/A-induced muscle paralysis were assessed by quantitative monitoring of muscle tension and digit abduction via the digit abduction scoring (DAS) assay. A single administration of ouabain significantly prolonged BoNT/A-induced neuromuscular... |
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Palavras-chave: Ouabain; Botulinum neurotoxin; Muscle atrophy; MAFbx; MuRF-1. |
Ano: 2010 |
URL: http://ir.obihiro.ac.jp/dspace/handle/10322/3123 |
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Padilha,A.S.; Salaices,M.; Vassallo,D.V.; Batista,P.R.; Siman,F.D.M.. |
Ouabain, an endogenous digitalis compound, has been detected in nanomolar concentrations in the plasma of several mammals and is associated with the development of hypertension. In addition, plasma ouabain is increased in several hypertension models, and the acute or chronic administration of ouabain increases blood pressure in rodents. These results suggest a possible association between ouabain and the genesis or development and maintenance of arterial hypertension. One explanation for this association is that ouabain binds to the α-subunit of the Na+ pump, inhibiting its activity. Inhibition of this pump increases intracellular Na+, which reduces the activity of the sarcolemmal Na+/Ca2+ exchanger and thereby reduces Ca2+ extrusion. Consequently,... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Ouabain; Hypertension; Vascular reactivity; Renin-angiotensin system. |
Ano: 2011 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2011000900015 |
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On the basis of our report that a glycolipoprotein fraction (GLP) extracted from Leptospira interrogans contains a potent inhibitor of renal Na,K-ATPase, we proposed that GLP-induced inhibition of Na,K-ATPase might be the primary cellular defect in the physiopathology of leptospirosis. The present study was designed to test this hypothesis by determining whether or not 1) GLP inhibits all the isoforms of Na,K-ATPase which are expressed in the tissues affected by leptospirosis, 2) Na,K-ATPase from leptospirosis-resistant species, such as the rat, is sensitive to GLP, 3) GLP inhibits Na,K-ATPase from intact cells, and 4) GLP inhibits ouabain-sensitive H,K-ATPase. The results indicate that in the rabbit, a leptospirosis-sensitive species, GLP inhibits with... |
Tipo: Info:eu-repo/semantics/other |
Palavras-chave: Na/K-ATPase; H/K-ATPase; Na/K-ATPase isoforms; Rubidium transport; Leptospirosis; Ouabain. |
Ano: 1997 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X1997000200009 |
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Giachini,F.R.C.; Carneiro,F.S.; Lima,V.V.; Carneiro,Z.N.; Brands,M.W.; Webb,R.C.; Tostes,R.C.. |
Oscillatory contractile activity is an inherent property of blood vessels. Various cellular mechanisms have been proposed to contribute to oscillatory activity. Mouse small mesenteric arteries display a unique low frequency contractile oscillatory activity (1 cycle every 10-12 min) upon phenylephrine stimulation. Our objective was to identify mechanisms involved in this peculiar oscillatory activity. First-order mesenteric arteries were mounted in tissue baths for isometric force measurement. The oscillatory activity was observed only in vessels with endothelium, but it was not blocked by L-NAME (100 µM) or indomethacin (10 µM), ruling out the participation of nitric oxide and prostacyclin, respectively, in this phenomenon. Oscillatory activity was not... |
Tipo: Info:eu-repo/semantics/article |
Palavras-chave: Oscillatory activity; Na+/K+-ATPase pump; Ouabain; Small mesenteric arteries. |
Ano: 2009 |
URL: http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2009001100010 |
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Registros recuperados: 10 | |
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