Knockout of the Na,K-ATPase α2-isoform in cardiac myocytes delays pressure overload-induced cardiac dysfunction

Knockout of the Na,K-ATPase α2-isoform in the cardiovascular system does not alter basal blood pressure but prevents ACTH-induced hypertension

(2011) Tara N. Rindler et al.   AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY

Hypertension from chronic central sodium chloride in mice is mediated by the ouabain-binding site on the Na,K-ATPase α2-isoform

(2011) James W. Van Huysse et al.   AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY

Mice expressing ouabain-sensitive α1-Na,K-ATPase have increased susceptibility to pressure overload-induced cardiac hypertrophy

(2010) Arshani N. Wansapura et al.   AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY

The central role of the brain aldosterone–“ouabain” pathway in salt-sensitive hypertension

(2010) Frans H.H. Leenen   BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

Molecular and Functional Characterization of a Novel Cardiac-Specific Human Tropomyosin Isoform

(2010) Sudarsan Rajan et al.   CIRCULATION

Extracellular potassium dependence of the Na+-K+-ATPase in cardiac myocytes: isoform specificity and effect of phospholemman

(2009) Fei Han et al.   AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY

Enhanced pressor response to increased CSF sodium concentration and to central ANG I in heterozygous α2 Na+-K+-ATPase knockout mice

(2009) Xiaohong Hou et al.   AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY

ACTH-induced hypertension is dependent on the ouabain-binding site of the α2-Na+-K+-ATPase subunit

(2008) John N. Lorenz et al.   AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY