ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit. - Wikidata - wikimedia - TriplyDB

ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit.

ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit.

http://www.wikidata.org/entity/Q36807967

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Specialized Functional Diversity and Interactions of the Na,K-ATPase Salt sensitivity, endogenous ouabain and hypertension Na+/Ca2+ exchange and Na+/K+-ATPase in the heart Na+-K+-ATPase, a new class of plasma membrane receptors Ouabain-digoxin antagonism in rat arteries and neurones Sodium 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 hypertrophy The ouabain-binding site of the α2 isoform of Na,K-ATPase plays a role in blood pressure regulation during pregnancy Endogenous cardiotonic steroids: physiology, pharmacology, and novel therapeutic targets.Endogenous ouabain: a link between sodium intake and hypertension Renovascular hypertension using a modified two-kidney, one-clip approach in mice is not dependent on the α1 or α2 Na-K-ATPase ouabain-binding site Endogenous 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-ATPase Activation of c-SRC underlies the differential effects of ouabain and digoxin on Ca(2+) signaling in arterial smooth muscle cells Knockout 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-ATPase Salt 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.

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P2860

ACTH-induced hypertension is dependent on the ouabain-binding site of the alpha2-Na+-K+-ATPase subunit.

http://www.wikidata.org/entity/Q36807967

description

2008 nî lūn-bûn

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2008年の論文

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ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.

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ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.

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ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.

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ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.

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AJPHEART.00183.2008

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American Journal of Physiology - Heart and Circulatory Physiology

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ACTH-induced hypertension is d ...... alpha2-Na+-K+-ATPase subunit.

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Elizabeth L Loreaux

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Iva Dostanic-Larson

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J Renee Schnetzer

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Jerry B Lingrel

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John N Lorenz

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Richard J Paul

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Valerie Lasko

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P2860

Haemodynamic mechanisms of corticotropin (ACTH)-induced hypertension in the rat

Uroguanylin knockout mice have increased blood pressure and impaired natriuretic response to enteral NaCl load

The alpha 1 isoform of Na,K-ATPase regulates cardiac contractility and functionally interacts and co-localizes with the Na/Ca exchanger in heart

The highly conserved cardiac glycoside binding site of Na,K-ATPase plays a role in blood pressure regulation

Targeted ablation of the phospholamban gene is associated with a marked decrease in sensitivity in aortic smooth muscle

Impact of psychological factors on the pathogenesis of cardiovascular disease and implications for therapy.

Glucocorticoid-induced hypertension: from mouse to man.

A practical guide to evaluating cardiovascular, renal, and pulmonary function in mice.

Na,K-ATPase: isoform structure, function, and expression.

Physiological role of the alpha1- and alpha2-isoforms of the Na+-K+-ATPase and biological significance of their cardiac glycoside binding site.

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2494766

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