Dietary Salt Exacerbates Isoproterenol-Induced Cardiomyopathy in Rats
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D. Costa | M. Willis | A. Nyska | N. Haykal-Coates | A. Farraj | M. Hazari | Alex P Carll | D. Winsett | J. Richards | A. Carll
[1] D. Costa,et al. Merits of Non-Invasive Rat Models of Left Ventricular Heart Failure , 2011, Cardiovascular Toxicology.
[2] A. Ledbetter,et al. Particulate matter inhalation exacerbates cardiopulmonary injury in a rat model of isoproterenol-induced cardiomyopathy , 2010, Inhalation toxicology.
[3] D. Takeshita,et al. Isoproterenol-induced hypertrophied rat hearts: does short-term treatment correspond to long-term treatment? , 2008, The journal of physiological sciences : JPS.
[4] D. Su,et al. PRESSOR AND NON‐PRESSOR EFFECTS OF SODIUM LOADING ON STROKE IN STROKE‐PRONE SPONTANEOUSLY HYPERTENSIVE RATS , 2008, Clinical and experimental pharmacology & physiology.
[5] G. Dorn,et al. Decompensation of cardiac hypertrophy: cellular mechanisms and novel therapeutic targets. , 2007, Physiology.
[6] M. Jokinen,et al. Characterization of spontaneous and chemically induced cardiac lesions in rodent model systems , 2007, Cardiovascular Toxicology.
[7] A. Ledbetter,et al. Neurotrophin mediation of allergic airways responses to inhaled diesel particles in mice. , 2006, Toxicological sciences : an official journal of the Society of Toxicology.
[8] E. Frohlich,et al. Myocardial fibrosis, impaired coronary hemodynamics, and biventricular dysfunction in salt-loaded SHR. , 2006, American journal of physiology. Heart and circulatory physiology.
[9] Claudio Passino,et al. Cardiac endocrine function is an essential component of the homeostatic regulation network: physiological and clinical implications. , 2006, American journal of physiology. Heart and circulatory physiology.
[10] David R Buvat de Virginy. Novel and potential future biomarkers for assessment of the severity and prognosis of chronic heart failure : a clinical review. , 2006, Heart failure reviews.
[11] C. Elangbam. Heart Trimming Protocol of the Laboratory Rat, Version 2, CD-ROM, Abraham Nyska, Beth Mahler, and Robert Maronpot , 2005, Toxicologic pathology.
[12] J. Krieger,et al. Chronic beta-adrenoceptor stimulation and cardiac hypertrophy with no induction of circulating renin. , 2005, European journal of pharmacology.
[13] P. Lechat,et al. Inhibition of Catecholamine-Induced Cardiac Fibrosis by an Aldosterone Antagonist , 2005, Journal of cardiovascular pharmacology.
[14] A. Nishiyama,et al. Cardiac oxidative stress in acute and chronic isoproterenol-infused rats. , 2005, Cardiovascular research.
[15] H. Iwao,et al. Additive beneficial effects of the combination of a calcium channel blocker and an angiotensin blocker on a hypertensive rat-heart failure model. , 2004, Hypertension research : official journal of the Japanese Society of Hypertension.
[16] E. Frohlich,et al. Cardiac structural and functional responses to salt loading in SHR. , 2004, American journal of physiology. Heart and circulatory physiology.
[17] M. Hamon,et al. Blockade of β1- and desensitization of β2-adrenoceptors reduce isoprenaline-induced cardiac fibrosis , 2004 .
[18] S. de Denus,et al. Brain natriuretic peptide in the management of heart failure: the versatile neurohormone. , 2004, Chest.
[19] M. Hamon,et al. Blockade of beta 1- and desensitization of beta 2-adrenoceptors reduce isoprenaline-induced cardiac fibrosis. , 2004, European journal of pharmacology.
[20] B. Persson,et al. Adrenergic mechanisms during hypertension induced by sucrose and/or salt in the spontaneously hypertensive rat , 2004, Naunyn-Schmiedeberg's Archives of Pharmacology.
[21] M. Klapholz,et al. Natriuretic peptides: biochemistry, physiology, and therapeutic role in heart failure. , 2003, Heart disease.
[22] G. Norton,et al. &bgr;-Adrenergic Activation Initiates Chamber Dilatation in Concentric Hypertrophy , 2003, Hypertension.
[23] E. Blasi,et al. Structural, functional, and molecular characterization of the SHHF model of heart failure. , 2002, American journal of physiology. Heart and circulatory physiology.
[24] J. Towbin,et al. The failing heart , 2002, Nature.
[25] D. Schlenk,et al. Toxic responses of the nervous system , 2001 .
[26] B. Chandrasekar,et al. Expression-Adrenergic Stimulation Induces Myocardial Proinflammatory Cytokine β Chronic , 2000 .
[27] M. Donowitz,et al. NHE2 contains subdomains in the COOH terminus for growth factor and protein kinase regulation. , 1999, American journal of physiology. Cell physiology.
[28] H. Thai,et al. Effects of AT1 receptor blockade after myocardial infarct on myocardial fibrosis, stiffness, and contractility. , 1999, American journal of physiology. Heart and circulatory physiology.
[29] A. Gerdes,et al. Gender-related differences in myocyte remodeling in progression to heart failure. , 1999, Hypertension.
[30] R. Willette,et al. The myocardial beta-adrenergic system in spontaneously hypertensive heart failure (SHHF) rats. , 1999, Hypertension.
[31] C. Johnston,et al. Salt induces myocardial and renal fibrosis in normotensive and hypertensive rats. , 1998, Circulation.
[32] R. Hernández-Muñoz,et al. Sequential changes of energy metabolism and mitochondrial function in myocardial infarction induced by isoproterenol in rats: a long-term and integrative study. , 1997, Canadian journal of physiology and pharmacology.
[33] E. Gelfand,et al. Noninvasive measurement of airway responsiveness in allergic mice using barometric plethysmography. , 1997, American journal of respiratory and critical care medicine.
[34] P. Singal,et al. Role of oxidative stress in transition of hypertrophy to heart failure. , 1996, Journal of the American College of Cardiology.
[35] E. Lakatta,et al. The ageing spontaneously hypertensive rat as a model of the transition from stable compensated hypertrophy to heart failure. , 1995, European heart journal.
[36] G. Wambach,et al. BNP plasma levels during acute volume expansion and chronic sodium loading in normal men. , 1995, Clinical and experimental hypertension.
[37] P. Singal,et al. Antioxidant changes in hypertrophied and failing guinea pig hearts. , 1994, The American journal of physiology.
[38] D. Das,et al. Molecular adaptation of cellular defences following preconditioning of the heart by repeated ischaemia. , 1993, Cardiovascular research.
[39] K. Weber,et al. Pathologic hypertrophy with fibrosis: the structural basis for myocardial failure. , 1992, Blood pressure.
[40] N. Minamino,et al. Increased plasma brain natriuretic peptide levels in DOCA-salt hypertensive rats: relation to blood pressure and cardiac concentration. , 1990, Biochemical and biophysical research communications.
[41] P. Baker,et al. SHHF/Mcc-cp Rat: Model of Obesity, Non-insulin-dependent Diabetes, and Congestive Heart Failure , 1990 .
[42] J. Mészáros,et al. Ultrastructural and electrophysiological alterations during the development of catecholamine-induced cardiac hypertrophy and failure. , 1990, Acta biologica Hungarica.
[43] P. Singal,et al. Higher Antioxidative Capacity During a Chronic Stable Heart Hypertrophy , 1989, Circulation research.
[44] M. Fujishima,et al. Central and peripheral mechanisms of the enhanced hypertension following long-term salt loading in spontaneously hypertensive rats. , 1988, Japanese circulation journal.
[45] M. Elam,et al. Chronic salt loading and central adrenergic mechanisms in the spontaneously hypertensive rat. , 2009, Acta pharmacologica et toxicologica.
[46] G. Rona. Catecholamine cardiotoxicity. , 1985, Journal of molecular and cellular cardiology.
[47] J. Milei,et al. A routine method for diagnosis of early myocardial infarction. , 1983, International journal of cardiology.
[48] R. Jaskot,et al. An automated analysis of glutathione peroxidase, S-transferase, and reductase activity in animal tissue. , 1983, Journal of analytical toxicology.
[49] S. Koletsky. Pathologic findings and laboratory data in a new strain of obese hypertensive rats. , 1975, The American journal of pathology.
[50] D. Spodick. Mechanisms of Contraction of the Normal and Failing Heart , 1968 .
[51] J. Ross,et al. Mechanisms of Contraction of the Normal and Failing Heart , 1969, The New England journal of medicine.