BACKGROUND: An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with differences in the plasma levels of ACE as well as with myocardial infarction, cardiomyopathy, left ventricular hypertrophy, and coronary artery disease. METHODS AND RESULTS: We determined the cardiac ACE activity and the ACE genotype in 71 subjects who died of noncardiac disorders. Cardiac ACE activity was significantly higher (P < .01) in subjects with the ACE DD genotype (12.7 +/- 1.9 mU/g wet wt) compared with subjects with the ID (8.7 +/- 0.8 mU/g) and the II (9.1 +/- 1.0 mU/g) genotypes. This difference was independent of sex, age, and the time required for tissue collection. CONCLUSIONS: Cardiac ACE activity is highest in subjects with the DD genotype. Elevated cardiac ACE activity in these subjects may result in increased cardiac angiotensin II levels, and this may be a mechanism underlying the reported association between the ACE deletion polymorphism and the increased risk for several cardiovascular disorders.
BACKGROUND: An insertion (I)/deletion (D) polymorphism of the angiotensin-converting enzyme (ACE) gene has been associated with differences in the plasma levels of ACE as well as with myocardial infarction, cardiomyopathy, left ventricular hypertrophy, and coronary artery disease. METHODS AND RESULTS: We determined the cardiac ACE activity and the ACE genotype in 71 subjects who died of noncardiac disorders. Cardiac ACE activity was significantly higher (P < .01) in subjects with the ACE DD genotype (12.7 +/- 1.9 mU/g wet wt) compared with subjects with the ID (8.7 +/- 0.8 mU/g) and the II (9.1 +/- 1.0 mU/g) genotypes. This difference was independent of sex, age, and the time required for tissue collection. CONCLUSIONS: Cardiac ACE activity is highest in subjects with the DD genotype. Elevated cardiac ACE activity in these subjects may result in increased cardiac angiotensin II levels, and this may be a mechanism underlying the reported association between the ACE deletion polymorphism and the increased risk for several cardiovascular disorders.
Authors: M A Qadar Pasha; Amjad P Khan; Ratan Kumar; Rekh B Ram; Surinder K Grover; Kaushal K Srivastava; William Selvamurthy; Samir K Brahmachari Journal: J Biosci Date: 2002-02 Impact factor: 1.826
Authors: Hedi Schelleman; Bruno H Ch Stricker; Anthonius De Boer; Abraham A Kroon; Monique W M Verschuren; Cornelia M Van Duijn; Bruce M Psaty; Olaf H Klungel Journal: Drugs Date: 2004 Impact factor: 9.546
Authors: Davide Seripa; Giulia Paroni; Maria G Matera; Carolina Gravina; Carlo Scarcelli; Michele Corritore; Luigi P D'Ambrosio; Maria Urbano; Grazia D'Onofrio; Massimiliano Copetti; Patrick G Kehoe; Francesco Panza; Alberto Pilotto Journal: Age (Dordr) Date: 2010-11-13
Authors: G Tsianos; K I Eleftheriou; E Hawe; L Woolrich; M Watt; I Watt; A Peacock; H Montgomery; S Grant Journal: Eur J Appl Physiol Date: 2004-12-01 Impact factor: 3.078
Authors: David Woods; Julie Sanders; Alun Jones; Emma Hawe; Peter Gohlke; Steve E Humphries; John Payne; Hugh Montgomery Journal: Eur J Appl Physiol Date: 2003-11-01 Impact factor: 3.078