O gene do angiotensinogênio (M235T) e o infarto agudo do miocárdio

Araújo, Messias Antônio; Menezes, Bruno Soares; Lourenço, Clauber; Cordeiro, Elisângela Rosa; Gatti, R; Goulart, Luiz Ricardo

doi:10.1590/s0104-42302005000300018

Cited by 7 publications

(8 citation statements)

References 16 publications

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“…The genomic region of the polymorphisms considered for investigation during this study were amplified by PCR with the following primers for AGT FW 5¢-GGA AGG ACA AGA ACT GCA CCT C-3¢ and RV 5¢-CAG GGT GCT GTC CAC ACT GGA CCC C-3¢ 12 and for ACE FW 5¢-CYG GAG ACC ACT CCC ATC CTT TCT-3¢ and RV 5¢-GAT GTG GCC ATC ACA TTC GTC AGA T-3¢. 13 To verify the ACE allelic distribution throughout the cohort, 1.5% agarose was employed.…”

Section: Methodsmentioning

confidence: 99%

Exaggerated blood pressure response during exercise treadmill testing: functional and hemodynamic features, and risk factors

et al. 2012

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The factors which contribute to an exaggerated blood pressure response (EBPR) during the exercise treadmill test (ETT) are not wholly understood. The association between the insertion/deletion polymorphisms of the angiotensin-converting enzyme (ACE) and M235T of the angiotensinogen with EBPR during ETT still remains unstudied. To identify and compare the risk factors for hypertension between normotensive subjects with EBPR and those who exhibit a normal curve of blood pressure (BP) during ETT. In a series of EBPR cases from a historical cohort of normotensive individuals, a univariate analysis was performed to estimate the association of the studied factors with BP behavior during ETT. Additionally, logistic multivariate regression was conducted to analyze the joint effects of the variables. P-values above 0.05 were considered statistically significant. From a total of 10 027 analyzed examinations, only 219 met the criteria employed to define EBPR, which resulted in a prevalence of 12.6%. For the systolic component of the BP, hyperreactive subjects displayed a mean age and body mass index (BMI) significantly higher than the others (P¼0.002 and o0.001, respectively). No association was observed between the polymorphisms cited above and EBPR. An analysis of the joint effect of variables has indicated that only age (Po 0.001) and BMI (P¼0.001) were specifically associated with systolic BP during exercise. Age and BMI were the only factors that independently influenced EBPR during ETT.

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Section: Methodsmentioning

confidence: 99%

Exaggerated blood pressure response during exercise treadmill testing: functional and hemodynamic features, and risk factors

et al. 2012

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“…TT homozygote individuals have plasma AGT levels 10 to 20% higher than MM homozygotes, thus showing a close association between that polymorphism and AGT plasma levels 18,26,27 . The positive correlation between polymorphism M235T and AGT plasma concentration has been observed in different populations [28][29][30] .…”

Section: Hypertension and Renin-angiotensin System Polymorphismsmentioning

confidence: 96%

Sistema renina-angiotensina: é possível identificar genes de suscetibilidade à hipertensão?

Lima¹,

Hatagima²,

Silva³

2007

Arq. Bras. Cardiol.

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“…For instance, the T allele of Met235Thr polymorphism of the AGT has been associated with systemic arterial hypertension (SAH). [8][9][10][11][12][13] Another genetic variant that could become a potential candidate marker for hypertension development is the NOS3 Glu298Asp. [14][15][16][17] Studies demonstrated that the A allele of the NOS3 gene is more susceptible to proteolytic cleavage in endothelial cells and vascular tissues, which might result in reduced levels of functional eNOS and may explain the possible mechanism that interferes in the enzyme function.…”

Section: Thismentioning

confidence: 99%

The interaction ofAGTandNOS3gene polymorphisms with conventional risk factors increases predisposition to hypertension

Gatti

Santos

Sena

et al. 2012

J Renin Angiotensin Aldosterone Syst

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Renin-angiotensin and kallikrein-kinin systems are interconnected, regulating blood pressure homeostasis. We have demonstrated the interactions among polymorphisms of the angiotensinogen (AGT) and endothelial nitric oxide synthase (NOS3) genes and conventional risk factors affecting the hypertension occurrence. Individuals were recruited (n=192) and classified into hypertensive (HG; n=140) and normotensive (NG; n=52) groups. The genotypic distribution of the Met235Thr (AGT) and Glu298Asp (NOS3) polymorphisms demonstrated that both are independent risk factors of hypertension (p=0.02 and p=0.008, respectively). The concomitant presence of these polymorphisms in the HG group was significantly different (p=0.001) from the NG. Both gene polymorphisms presented an additive effect for the unfavourable alleles T and A, respectively, and 95% of the double mutant homozygotes were classified into the HG. Specific interactions among certain conventional factors and the presence of at least one unfavourable allele presented significant odds towards hypertension. Blood pressure homeostasis was affected by genetic polymorphisms conditioned by the T and A alleles of the AGT and NOS3 genes, respectively, which acted independently. However, their interaction with smoking, sedentariness, age and total cholesterol may have increased the predisposition to hypertension, which may explain most of the hypertension cases.

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O gene do angiotensinogênio (M235T) e o infarto agudo do miocárdio

Abstract: No association was found between the angiotensinogen gene M235T polymorphism and coronary artery disease, neither with its severity nor with acute myocardial infarction.

Cited by 7 publications

References 16 publications

Exaggerated blood pressure response during exercise treadmill testing: functional and hemodynamic features, and risk factors

Exaggerated blood pressure response during exercise treadmill testing: functional and hemodynamic features, and risk factors

Sistema renina-angiotensina: é possível identificar genes de suscetibilidade à hipertensão?

The interaction ofAGTandNOS3gene polymorphisms with conventional risk factors increases predisposition to hypertension

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