Transgenic alpha1A-adrenergic activation limits post-infarct ventricular remodeling and dysfunction and improves survival.

[1]  L. Tecott,et al.  Alpha1-adrenergic receptors prevent a maladaptive cardiac response to pressure overload. , 2006, The Journal of clinical investigation.

[2]  R. Graham,et al.  Sustained augmentation of cardiac alpha1A-adrenergic drive results in pathological remodeling with contractile dysfunction, progressive fibrosis and reactivation of matricellular protein genes. , 2006, Journal of molecular and cellular cardiology.

[3]  N. Maeda,et al.  The role of natriuretic peptides in cardioprotection. , 2006, Cardiovascular research.

[4]  W. Burns,et al.  Connective Tissue Growth Factor and Cardiac Fibrosis after Myocardial Infarction , 2005, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[5]  A. Dart,et al.  Mouse model of post-infarct ventricular rupture: time course, strain- and gender-dependency, tensile strength, and histopathology. , 2005, Cardiovascular research.

[6]  R. Graham,et al.  Genetic enhancement of ventricular contractility protects against pressure-overload-induced cardiac dysfunction. , 2004, Journal of molecular and cellular cardiology.

[7]  P. Doevendans,et al.  Connective tissue growth factor expression and Smad signaling during mouse heart development and myocardial infarction , 2004, Developmental dynamics : an official publication of the American Association of Anatomists.

[8]  J. Chrast,et al.  Chronic phospholamban inhibition prevents progressive cardiac dysfunction and pathological remodeling after infarction in rats. , 2004, The Journal of clinical investigation.

[9]  P. Doevendans,et al.  MCIP1 Overexpression Suppresses Left Ventricular Remodeling and Sustains Cardiac Function After Myocardial Infarction , 2004, Circulation research.

[10]  M. Pfeffer,et al.  Post-myocardial infarction ventricular remodeling: Animal and human studies , 1994, Cardiovascular Drugs and Therapy.

[11]  L. Wilkins.  Diuretic Versus &agr;-Blocker as First-Step Antihypertensive Therapy: Final Results From the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) , 2003 .

[12]  J. Boehmer.  Device therapy for heart failure. , 2003, The American journal of cardiology.

[13]  Xiao-Ming Gao,et al.  Increased myocardial collagen and ventricular diastolic dysfunction in relaxin deficient mice: a gender-specific phenotype. , 2003, Cardiovascular research.

[14]  B. Hoit,et al.  Hypertrophy and functional alterations in hyperdynamic phospholamban-knockout mouse hearts under chronic aortic stenosis. , 2002, Cardiovascular research.

[15]  C. O'connor,et al.  Inotropic therapy for heart failure: an evidence-based approach. , 2001, American heart journal.

[16]  R. Graham,et al.  Targeted &agr;1A-Adrenergic Receptor Overexpression Induces Enhanced Cardiac Contractility but not Hypertrophy , 2001, Circulation research.

[17]  A. Ducharme,et al.  Cardiac-directed overexpression of wild-type alpha1B-adrenergic receptor induces dilated cardiomyopathy. , 2001, American journal of physiology. Heart and circulatory physiology.

[18]  A. Dart,et al.  Preserved ventricular contractility in infarcted mouse heart overexpressing beta(2)-adrenergic receptors. , 2000, American journal of physiology. Heart and circulatory physiology.

[19]  E. Woodcock,et al.  β2-Adrenergic receptor overexpression driven by α-MHC promoter is downregulated in hypertrophied and failing myocardium , 2000 .

[20]  R. Lefkowitz,et al.  Preservation of myocardial β-adrenergic receptor signaling delays the development of heart failure after myocardial infarction , 2000 .

[21]  G. Dorn,et al.  Early and delayed consequences of beta(2)-adrenergic receptor overexpression in mouse hearts: critical role for expression level. , 2000, Circulation.

[22]  M. Bristow.  β-Adrenergic Receptor Blockade in Chronic Heart Failure , 2000 .

[23]  A. Dart,et al.  Serial echocardiographic assessment of left ventricular dimensions and function after myocardial infarction in mice. , 2000, Cardiovascular research.

[24]  A. Dart,et al.  beta(2)-adrenergic receptor overexpression exacerbates development of heart failure after aortic stenosis. , 2000, Circulation.

[25]  M. Martone,et al.  Chronic Phospholamban–Sarcoplasmic Reticulum Calcium ATPase Interaction Is the Critical Calcium Cycling Defect in Dilated Cardiomyopathy , 1999, Cell.

[26]  M. Lohse,et al.  Progressive hypertrophy and heart failure in beta1-adrenergic receptor transgenic mice. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[27]  M. Bristow.  Mechanism of action of beta-blocking agents in heart failure. , 1997, The American journal of cardiology.

[28]  G. Lamas,et al.  Cardiovascular death and left ventricular remodeling two years after myocardial infarction: baseline predictors and impact of long-term use of captopril: information from the Survival and Ventricular Enlargement (SAVE) trial. , 1997, Circulation.

[29]  S. Solomon,et al.  Early versus delayed angiotensin-converting enzyme inhibition therapy in acute myocardial infarction. The healing and early afterload reducing therapy trial. , 1997, Circulation.

[30]  Y. Ishikawa,et al.  Overexpression of Gs alpha protein in the hearts of transgenic mice. , 1995, The Journal of clinical investigation.

[31]  M. Pfeffer.  Left ventricular remodeling after acute myocardial infarction. , 1995, Annual review of medicine.

[32]  R. Lefkowitz,et al.  Myocardial expression of a constitutively active alpha 1B-adrenergic receptor in transgenic mice induces cardiac hypertrophy. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[33]  R. Lefkowitz,et al.  Enhanced myocardial function in transgenic mice overexpressing the beta 2-adrenergic receptor. , 1994, Science.

[34]  Regional remodeling and nonuniform changes in diastolic function in patients with left ventricular dysfunction: modification by long-term enalapril treatment. The SOLVD Investigators. , 1993, Journal of the American College of Cardiology.

[35]  E. Shapiro,et al.  Myocardial infarct expansion: recognition, significance and pathology. , 1991, The American journal of cardiology.

[36]  O Muzik,et al.  Assessment of myocardial perfusion by positron emission tomography. , 1991, The American journal of cardiology.

[37]  P. Simpson,et al.  Stimulation of hypertrophy of cultured neonatal rat heart cells through an alpha 1-adrenergic receptor and induction of beating through an alpha 1- and beta 1-adrenergic receptor interaction. Evidence for independent regulation of growth and beating. , 1985, Circulation research.

[38]  P. Simpson.  Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha 1 adrenergic response. , 1983, The Journal of clinical investigation.