Angiotensin II type 1 receptor A1166C gene polymorphism Absence of an association with the risk of coronary artery disease and myocardial infarction and of a synergistic effect with angiotensin-converting enzyme gene polymorphism on the risk of these diseases

Gardemann, Andreas; Nguyên, Quôc Dinh; Humme, Jörg; Stricker, Jürgen; Katz, Norbert; Tillmanns, Harald; Hehrlein, F. W.; Rau, Matthias; Haberbosch, Werner

doi:10.1053/euhj.1998.1097

Cited by 49 publications

(36 citation statements)

References 37 publications

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“…9 However, as with the ACE polymorphism, others have found no association with hypertension 20 -22 and coronary artery disease. 23,24 These conflicting data can be caused by differences in selection criteria of the sample, ethnic diversity, or the often retrospective or cross-sectional nature of the analyses. Because most of the polymorphic markers in the RAS confer a low absolute risk, it is very important to specify a possible stable phenotype that elucidates the relative role of a polymorphism in cardiovascular disease.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Type 1 Receptor A1166C Gene Polymorphism Is Associated With an Increased Response to Angiotensin II in Human Arteries

et al. 2000

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Abstract-An adenine/cytosine (A/C) base substitution at position 1166 in the angiotensin II type 1 receptor (AT 1 R) gene is associated with the incidence of essential hypertension and increased coronary artery vasoconstriction. However, it is still unknown whether this polymorphism is associated with a difference in angiotensin II responsiveness. Therefore, we assessed whether the AT 1 R polymorphism is associated with different responses to angiotensin II in isolated human arteries. Furthermore, we evaluated whether inhibition of the renin-angiotensin system modifies the effect of the AT 1 R polymorphism. One hundred twelve patients who were undergoing coronary artery bypass graft surgery were prospectively randomized to receive an ACE inhibitor or a placebo for 1 week before surgery. Excess segments of the internal mammary artery were exposed to angiotensin II (0.1 nmol/L to 1 mol/L) and KCl (60 mmol/L) in organ bath experiments. Patients homozygous for the C allele (nϭ17) had significantly greater angiotensin II responses (percentage of this maximal KCl-induced response) than did patients genotyped with AAϩAC (nϭ95, PϽ0.05). Although ACE inhibition increased the response to angiotensin II, the difference in the response to angiotensin II, between CC and AAϩAC patients remained intact in ACE inhibitor-treated patients. These results indicate increased responses to angiotensin II in patients with the CC genotype. The mechanism is preserved during ACE inhibition, which in itself also increased the response to angiotensin II. This reveals that the A1166C polymorphism may be in linkage disequilibrium with a functional mutation that alters angiotensin II responsiveness, which may explain the described relation between this polymorphism and cardiovascular abnormalities.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II Type 1 Receptor A1166C Gene Polymorphism Is Associated With an Increased Response to Angiotensin II in Human Arteries

et al. 2000

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“…[23][24][25] No evidence of an association was detected between cardiovascular structural phenotype, either LV mass or carotid artery wall thickness, and A/C1166 polymorphism. 23 Hindorff et al have reported that A/C1166 polymorphism was not associated with blood pressure control or incident cardiovascular events.…”

Section: 7±04 Ns No Significant Difference Was Found Among Three Gementioning

confidence: 99%

Association Between A/C1166 Gene Polymorphism of the Angiotensin II Type 1 Receptor and Biventricular Functions in Patients With Acute Myocardial Infarction

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et al. 2006

Circ J

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cute myocardial infarction (AMI) is characterized by loss of contractile tissue and changes in ventricular geometry. 1 The presence of congestive heart failure or left ventricular (LV) systolic dysfunction is probably the most important risk factor in patients with AMI. 2 The development of right ventricular (RV) dysfunction has been reported following LV myocardial infarction (MI), 3,4 and is also associated with increased risk of shock, arrhythmia, and death. 5,6 After MI, the process of LV remodeling begins rapidly, usually within the first few hours after an infarct, and continues to progress. 7 Furthermore, it is known that the renin -angiotensin -aldosterone system (RAS) and angiotensin-converting enzyme (ACE) activity contribute to the remodeling process. 8 Angiotensin II (ATII) is the final effector of the RAS. It is a vasoactive peptide and leads to growth promotion, fibroblast proliferation, and the most potent vasoactive and salt-retaining effector peptide of the RAS, which is involved in blood pressure homeostasis and cardiovascular pathophysiology. Two subtypes of cell surface receptors, ATII type 1 receptor (AT1R) and ATII type 2 receptor Circulation Journal Vol. 70, October 2006 (AT2R), have been identified. Most of the actions of ATII are mediated by AT1, which is particularly prominent in the myocardium. 9,10 Although a number of polymorphisms of the AT1R gene have been identified, one of the most widely studied is an A-C substitution at position 1166 (A/C1166). 11 Two-dimensional (D) and Doppler echocardiography is a reliable tool for the diagnosis of systolic and diastolic dysfunction. The Doppler echocardiographic myocardial performance index (MPI) called the "Tei index", combining time intervals of LV contraction and relaxation, has been shown to be a powerful predictor of death and congestive heart failure after MI. 12,13 This index can be obtained easily, is reproducible and independent of the ventricular geometry, and has been shown to have potential for clinical application in the assessment of overall cardiac function in various disorders. 14 Poulsen et al recently reported that the LVMPI was a powerful predictor of death or congestive heart failure after MI, 15 and Moller et al showed that the RVMPI was increased in the acute phase of MI and was significantly correlated with indices of RV systolic dysfunction. 16 In a previous study, we reported higher LVMPI and RVMPI in patients with the DD genotype than in patients with the ID genotype of the ACE gene after anterior AMI. 17 Although there have been several association studies of the polymorphism of AT1R (A/C1166) in clinical endpoints, such as MI, 18 hypertension, 11 aortic stiffness, 19 and LV mass, 20 to our knowledge the relationship between AT1R polymorphism and biventricular function in anterior Methods and ResultsThe study group comprised 132 consecutive patients who were admitted to the coronary care unit with their first acute anterior MI. Systolic and diastolic diameters, volumes, inflow properties, ejection fraction an...

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“…As no polymorphism was detected that modified the encoded amino acid sequence (27), they further speculated that the AT1R C allele is in linkage disequilibrium with a functional variant that could alter the down regulation of/~T1R gene in response to All, which is present in increased concentration with ACE DD genotype. Similar kind of studies carried out, where the synergistic interaction between ACE DID and AT1R NC on MI was reported (39) while it was disapproved by others (40). AT1R C allele was also shown to be independently associated with CHD (41)(42)(43)).…”

Section: Angiotensin II Type I Receptor (Atir)mentioning

confidence: 63%

Genes of renin angiotensin system and coronary heart disease

Ashavaid

Shalia

Nair

et al. 2000

Indian J Clin Biochem

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Coronary constriction, proliferation of smooth muscle cells and arrhythmia are involved in the pathophysiology of coronary heart disease and its complications such as myocardial infarction and sudden death. All these effects are favoured by high angiotensin II levels. Angiotensin II is the main effector molecule of the renin angiotensin system and it acts through angiotensin II type receptors. Genetically determined differences in the expression of the components of this system could adversely affect angiotensin II concentration and subsequently heart. Consequently each component of this system represents a potential candidate in the etiology of cardiovascular disease. In this article we review the variation of the angiotensin I converting enzyme, angiotensin II type I receptor and angiotensinogen genes and their association with cardiovascular disease.

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Angiotensin II type 1 receptor A1166C gene polymorphism Absence of an association with the risk of coronary artery disease and myocardial infarction and of a synergistic effect with angiotensin-converting enzyme gene polymorphism on the risk of these diseases

Cited by 49 publications

References 37 publications

Angiotensin II Type 1 Receptor A1166C Gene Polymorphism Is Associated With an Increased Response to Angiotensin II in Human Arteries

Angiotensin II Type 1 Receptor A1166C Gene Polymorphism Is Associated With an Increased Response to Angiotensin II in Human Arteries

Association Between A/C1166 Gene Polymorphism of the Angiotensin II Type 1 Receptor and Biventricular Functions in Patients With Acute Myocardial Infarction

Genes of renin angiotensin system and coronary heart disease

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