ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit.
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Specialized Functional Diversity and Interactions of the Na,K-ATPaseSalt sensitivity, endogenous ouabain and hypertensionNa+/Ca2+ exchange and Na+/K+-ATPase in the heartNa+-K+-ATPase, a new class of plasma membrane receptorsOuabain-digoxin antagonism in rat arteries and neuronesSodium potassium adenosine triphosphatase (Na/K-ATPase) as a therapeutic target for uremic cardiomyopathy.Targeted mutations in the Na,K-ATPase α 2 isoform confer ouabain resistance and result in abnormal behavior in mice.Upregulation of Na+ and Ca2+ transporters in arterial smooth muscle from ouabain-induced hypertensive rats.Neuroendocrine humoral and vascular components in the pressor pathway for brain angiotensin II: a new axis in long term blood pressure control.Why isn't endogenous ouabain more widely accepted?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.Endogenous ouabain: a link between sodium intake and hypertensionRenovascular 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.How NaCl raises blood pressure: a new paradigm for the pathogenesis of salt-dependent hypertension.Arterial 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?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 cellsKnockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction.Novel role of transient receptor potential vanilloid 2 in the regulation of cardiac performance.The physiological significance of the cardiotonic steroid/ouabain-binding site of the Na,K-ATPaseSalt Sensitivity: Challenging and Controversial Phenotype of Primary Hypertension.Update on angiotensin II: new endocrine connections between the brain, adrenal glands and the cardiovascular system.Cross talk between plasma membrane Na(+)/Ca (2+) exchanger-1 and TRPC/Orai-containing channels: key players in arterial hypertension.Aldosterone and Mineralocorticoid Receptors-Physiology and Pathophysiology.Physiological roles of endogenous ouabain in normal rats.The C-terminal cavity of the Na,K-ATPase analyzed by docking and electrophysiology.How does pressure overload cause cardiac hypertrophy and dysfunction? High-ouabain affinity cardiac Na+ pumps are crucial.The pump, the exchanger, and the holy spirit: origins and 40-year evolution of ideas about the ouabain-Na+ pump endocrine system.Pivotal role of α2 Na+ pumps and their high affinity ouabain binding site in cardiovascular health and disease.The α2 isoform of the Na,K-pump is important for intercellular communication, agonist-induced contraction, and EDHF-like response in rat mesenteric arteries.
P2860
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P2860
ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit.
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.
@ast
ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.
@en
type
label
ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.
@ast
ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.
@en
prefLabel
ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.
@ast
ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.
@en
P2093
P2860
P1476
ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.
@en
P2093
Elizabeth L Loreaux
Iva Dostanic-Larson
J Renee Schnetzer
Jerry B Lingrel
John N Lorenz
Richard J Paul
Valerie Lasko
P2860
P304
P356
10.1152/AJPHEART.00183.2008
P577
2008-05-16T00:00:00Z