Effects of ACEI induced Cough on LV mass in Hypertensive patients and Its Reduction by Antihypertensive Medication
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Hae-Young Lee | Hyo‐Soo Kim | J. H. Lee | D. Sohn | M. Lee | S. Na | I. Chae | B. Oh | Young Bae Park | Jun Kyu Lee | Y. Lee | Y. Choi | Jun Kyu Lee | Youngwoo Lee | Y. Park | Yun Sik Choi | J. Lee
[1] T Kuznetsova,et al. Antihypertensive treatment modulates the association between the D/I ACE gene polymorphism and left ventricular hypertrophy: a meta-analysis , 2000, Journal of Human Hypertension.
[2] D. Sohn,et al. Synergistic effect of angiotensin-converting enzyme and angiotensinogen gene on cardiac hypertrophy. , 2000, International journal of cardiology.
[3] J. Yoshikawa,et al. Association between angiotensin-converting enzyme gene polymorphisms and regression of left ventricular hypertrophy in patients treated with angiotensin-converting enzyme inhibitors. , 1999, The American journal of medicine.
[4] F. Perticone,et al. Deletion polymorphism of angiotensin-converting enzyme gene and left ventricular hypertrophy in southern Italian patients. , 1997, Journal of the American College of Cardiology.
[5] A. Gharavi,et al. Deletion polymorphism of the angiotensin-converting enzyme gene is independently associated with left ventricular mass and geometric remodeling in systemic hypertension. , 1996, The American journal of cardiology.
[6] M. Quiñones,et al. Angiotensin-I converting enzyme genotypes and left ventricular hypertrophy in patients with hypertrophic cardiomyopathy. , 1995, Circulation.
[7] H. Schunkert,et al. Angiotensin-converting enzyme in the human heart. Effect of the deletion/insertion polymorphism. , 1995, Circulation.
[8] T. Parrish,et al. Bradykinin antagonism inhibits the antigrowth effect of converting enzyme inhibition in the dog myocardium after discrete transmural myocardial necrosis. , 1995, Circulation.
[9] H. Schunkert,et al. Association between a deletion polymorphism of the angiotensin-converting-enzyme gene and left ventricular hypertrophy. , 1994, The New England journal of medicine.
[10] Y. Kawakami,et al. Angiotensin-I-converting enzyme gene polymorphism and susceptibility to cough , 1994, The Lancet.
[11] J. Sadoshima,et al. Critical Role of the AT1 Receptor Subtype , 2005 .
[12] D. Ganten,et al. Selective activation of cardiac angiotensinogen gene expression in post-infarction ventricular remodeling in the rat. , 1993, Journal of molecular and cellular cardiology.
[13] J. Imbs,et al. Cough and ACE inhibitors , 1993, The Lancet.
[14] Philippe Amouyel,et al. Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction , 1992, Nature.
[15] F. Soubrier,et al. PCR detection of the insertion/deletion polymorphism of the human angiotensin converting enzyme gene (DCP1) (dipeptidyl carboxypeptidase 1). , 1992, Nucleic acids research.
[16] E. J. Martinez,et al. Respiratory Tract Side Effects of Angiotensin Converting Enzyme Inhibitors: Current Knowledge , 1991, Southern medical journal.
[17] A. Morice,et al. ACE inhibitor cough: a genetic link? , 1991, The Lancet.
[18] P Corvol,et al. An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. , 1990, The Journal of clinical investigation.
[19] K. Baker,et al. Angiotensin II stimulation of protein synthesis and cell growth in chick heart cells. , 1990, The American journal of physiology.
[20] D. Ganten,et al. Converting enzyme inhibition specifically prevents the development and induces regression of cardiac hypertrophy in rats. , 1989, Clinical and experimental hypertension. Part A, Theory and practice.
[21] R. Goldszer,et al. Prevalence of cough during angiotensin-converting enzyme inhibitor therapy. , 1988, The American journal of medicine.
[22] G. Lamas,et al. Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction. , 1988, The New England journal of medicine.
[23] A. LaCroix,et al. Electrocardiographic estimate of left ventricular mass versus radiographic cardiac size and the risk of cardiovascular disease mortality in the epidemiologic follow-up study of the First National Health and Nutrition Examination Survey. , 1988, The American journal of cardiology.
[24] J. Drazen,et al. Substance P-induced bronchoconstriction in the guinea pig. Enhancement by inhibitors of neutral metalloendopeptidase and angiotensin-converting enzyme. , 1988, The American review of respiratory disease.
[25] D. Coulter,et al. Cough associated with captopril and enalapril. , 1987, British medical journal.
[26] N. Thornberry,et al. Carboxyl-terminal tripeptidyl hydrolysis of substance P by purified rabbit lung angiotensin-converting enzyme and the potentiation of substance P activity in vivo by captopril and MK-422. , 1984, Molecular pharmacology.
[27] G. Williams,et al. Angiotensin-converting enzyme inhibition and prostaglandins. , 1982, The American journal of cardiology.
[28] M. Antonaccio,et al. The effects of captopril (SQ 14,225) on bradykinin-induced bronchoconstriction in the anesthetized guinea pig. , 1979, European journal of pharmacology.
[29] H. Coleridge,et al. Stimulation of ‘irritant’ receptors and afferent C-fibres in the lungs by prostaglandins , 1976, Nature.