The highly conserved cardiac glycoside binding site of Na,K-ATPase plays a role in blood pressure regulation
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Carbonylation Modification Regulates Na/K-ATPase Signaling and Salt Sensitivity: A Review and a HypothesisSpecialized Functional Diversity and Interactions of the Na,K-ATPaseNa+/Ca2+ exchange and Na+/K+-ATPase in the heartOuabain-digoxin antagonism in rat arteries and neuronesSodium potassium adenosine triphosphatase (Na/K-ATPase) as a therapeutic target for uremic cardiomyopathy.Knockout of Na+/Ca2+ exchanger in smooth muscle attenuates vasoconstriction and L-type Ca2+ channel current and lowers blood pressureRole of endosomal Na+-K+-ATPase and cardiac steroids in the regulation of endocytosis.Upregulation of Na+ and Ca2+ transporters in arterial smooth muscle from ouabain-induced hypertensive rats.Ouabain stimulates Na-K-ATPase through a sodium/hydrogen exchanger-1 (NHE-1)-dependent mechanism in human kidney proximal tubule cellsSignaling mechanisms that link salt retention to hypertension: endogenous ouabain, the Na(+) pump, the Na(+)/Ca(2+) exchanger and TRPC proteins.Intracellular calcium regulates nonsense-mediated mRNA decay.Endogenous cardiotonic steroids and salt-sensitive hypertension.The sodium pump and hypertension: a physiological role for the cardiac glycoside binding site of the Na,K-ATPase.Renal ischemia regulates marinobufagenin release in humans.Normal pregnancy: mechanisms underlying the paradox of a ouabain-resistant state with elevated endogenous ouabain, suppressed arterial sodium calcium exchange, and low blood pressureWhy isn't endogenous ouabain more widely accepted?A new clinical multivariable model that predicts postoperative acute kidney injury: impact of endogenous ouabainA key role for Na+/K+-ATPase in the endothelium-dependent oscillatory activity of mouse small mesenteric arteries.Mice expressing ouabain-sensitive α1-Na,K-ATPase have increased susceptibility to pressure overload-induced cardiac hypertrophyThe ouabain-binding site of the α2 isoform of Na,K-ATPase plays a role in blood pressure regulation during pregnancyEndogenous cardiotonic steroids: physiology, pharmacology, and novel therapeutic targets.Spherical Oligo-Silicic Acid SOSA Disclosed as Possible Endogenous Digitalis-Like Factor.Properties and expression of Na+/K+-ATPase α-subunit isoforms in the brain of the swamp eel, Monopterus albus, which has unusually high brain ammonia toleranceRenovascular hypertension using a modified two-kidney, one-clip approach in mice is not dependent on the α1 or α2 Na-K-ATPase ouabain-binding siteEndogenous digitalis-like factors: an overview of the history.Knockout of the Na,K-ATPase α₂-isoform in the cardiovascular system does not alter basal blood pressure but prevents ACTH-induced hypertension.Reactive Oxygen Species Modulation of Na/K-ATPase Regulates Fibrosis and Renal Proximal Tubular Sodium HandlingHow NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension.Increased arterial smooth muscle Ca2+ signaling, vasoconstriction, and myogenic reactivity in Milan hypertensive ratsArterial α2-Na+ pump expression influences blood pressure: lessons from novel, genetically engineered smooth muscle-specific α2 mice.Nanomolar ouabain increases NCX1 expression and enhances Ca2+ signaling in human arterial myocytes: a mechanism that links salt to increased vascular resistance?Ouabain-stimulated trafficking regulation of the Na/K-ATPase and NHE3 in renal proximal tubule cellsCritical role of the α1-Na(+), K(+)-ATPase subunit in insensitivity of rodent cells to cytotoxic action of ouabain.How does salt retention raise blood pressure?Physiological role of the alpha1- and alpha2-isoforms of the Na+-K+-ATPase and biological significance of their cardiac glycoside binding site.Relationships among endogenous ouabain, alpha-adducin polymorphisms and renal sodium handling in primary hypertension.DOCA-salt hypertension does not require the ouabain-sensitive binding site of the α2 Na,K-ATPaseActivation of c-SRC underlies the differential effects of ouabain and digoxin on Ca(2+) signaling in arterial smooth muscle cellsNew roles for an old enzyme: Na,K-ATPase emerges as an interesting drug target.Knockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction.
P2860
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P2860
The highly conserved cardiac glycoside binding site of Na,K-ATPase plays a role in blood pressure regulation
description
2005 nî lūn-bûn
@nan
2005 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
The highly conserved cardiac g ...... e in blood pressure regulation
@ast
The highly conserved cardiac g ...... e in blood pressure regulation
@en
The highly conserved cardiac g ...... e in blood pressure regulation
@nl
type
label
The highly conserved cardiac g ...... e in blood pressure regulation
@ast
The highly conserved cardiac g ...... e in blood pressure regulation
@en
The highly conserved cardiac g ...... e in blood pressure regulation
@nl
prefLabel
The highly conserved cardiac g ...... e in blood pressure regulation
@ast
The highly conserved cardiac g ...... e in blood pressure regulation
@en
The highly conserved cardiac g ...... e in blood pressure regulation
@nl
P2093
P2860
P921
P3181
P356
P1476
The highly conserved cardiac g ...... e in blood pressure regulation
@en
P2093
Iva Dostanic-Larson
James W Van Huysse
Jerry B Lingrel
John N Lorenz
P2860
P304
15845-15850
P3181
P356
10.1073/PNAS.0507358102
P407
P577
2005-10-21T00:00:00Z