Pressure-induced cardiac hypertrophy: changes in Na+, K+-ATPase and glycoside actions in cats
Author:
Publisher
Elsevier BV
Subject
Pharmacology
Reference18 articles.
1. Effects of cardiac glycosides on Na+, K+-ATPase;Akera,1981
2. A simple method for the determination of affinity and binding site concentration in receptor binding studies;Akera;Biochim. Biophys. Acta,1977
3. Chronic partial occlusion of the pulmonary artery in cats;Bassett;Circ. Res.,1973
4. Intact vesicles of canine cardiac sarcolemma: evidence from vectorial properties of Na+, K+-ATPase;Besch;Circ. Res.,1976
5. Myocardial necrosis, fibrosis, and DNA synthesis in experimental cardiac hypertrophy induced by sudden pressure overload;Bishop;Circ. Res.,1976
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1. Mechanisms underlying delayed afterdepolarizations in hypertrophied left ventricular myocytes of rats;American Journal of Physiology-Heart and Circulatory Physiology;2001-08-01
2. Increased digitalis-like immunoreactive substances in patients with hypertrophic cardiomyopathy;European Heart Journal;2000-02-15
3. Reductions of myocardial Na-K-ATPase activity and ouabain binding sites in heart failure: prevention by nadolol;American Journal of Physiology-Heart and Circulatory Physiology;1993-12-01
4. Effects of brief repetitive ischemia on contractility, relaxation, and coronary flow. Exaggerated postischemic diastolic dysfunction in pressure-overload hypertrophy.;Circulation Research;1993-09
5. Myocardial Na+,K+-ATPase in tachycardia induced cardiomyopathy;Journal of Molecular and Cellular Cardiology;1992-03
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