How ineffective hypertension control in subjects treated with angiotensin-converting enzyme inhibitors is related to polymorphisms in the renin-angiotensin-aldosterone system

Morales-Suárez-Varela, María; Mansego, María L.; Martı́n-Escudero, Juan Carlos; Llópis-González, Agustín; Chaves, Felipe Javier; López-Izquierdo, Raúl; Frutos-Llanes, Raul; Vicedo‐Cabrera, Ana M.

doi:10.1016/j.ejps.2010.01.007

Cited by 7 publications

(8 citation statements)

References 35 publications

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“…Recent pharmacogenomics advances have revealed that some gene variants of the RAAS are involved in the effectiveness of anti-AHT treatment, especially with angiotensin II receptor blockers or the ACE inhibitor response. 12,30 Indeed, this result could relate to our last study, where we found a possible association of the presence of certain polymorphisms of RAAS genes with the risk of uncontrolled HT in ACE inhibitor-treated patients. 12 As noted above and by Redon et al 6 the similarity between cases and controls in the consumption of anti-AHT drug types makes it difficult to prescribe treatments to control AHT.…”

Section: Discussionsupporting

confidence: 61%

“…The RAAS is an excellent candidate to investigate the genetic factors that control AHT in MS patients in relation to gene-environment interactions and their influence on the patients' health status. [10][11][12] For example, Milionis et al 5 observed a possible association of the AC genotype and the C allele of the angiotensin II type-1 receptor gene with a better response to structured anti-AHT treatment in MS patients.…”

Section: Introductionmentioning

confidence: 99%

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Inefficient arterial hypertension control in patients with metabolic syndrome and its link to renin–angiotensin–aldosterone system polymorphisms

Morales-Suárez-Varela

Mansego

Vicedo‐Cabrera

et al. 2011

Hypertens Res

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There is evidence that uncontrolled arterial hypertension (AHT) in patients with metabolic syndrome (MS) increases cardiovascular risks. The renin-angiotensin-aldosterone system (RAAS) and its polymorphisms apparently confer a genetic risk for uncontrolled AHT. This study aims to investigate the influence of RAAS polymorphisms on AHT control in patients diagnosed with MS. This is a two-stage population-based nested case-control pilot study (n¼1514). We differentiated between MS-diagnosed patients and non-MS patients (ATP-III criteria) and selected those individuals diagnosed with AHT from each group (n¼161 and n¼156, respectively). Those who successfully controlled their AHT (controls) and those who did not were compared. In the MS population, the C/G and G/G genotypes of single-nucleotide polymorphism rs1040288 (NR3C2) and A/G and G/G of rs11099680 (NR3C2) were associated with uncontrolled AHT (odds ratio (OR)¼2.94 (1.34-6.47) and OR¼2.54 (1.09-5.93), respectively). According to Akaike's information criteria, the best adjusted model included gender and age as confounding variables (adjusted OR (ORa)¼2.91 (1.31-6.46) and ORa¼2.67 (1.13-6.31), respectively). Regarding rs1040288, an ORa of 4.03 (1.44-11.26) was obtained for the saturated model (adjusted for gender, age, waist-to-hip ratio, body mass index, biochemical profile, renal damage, smoking habit and anti-AHT treatment). Yet, when the same analysis was performed on the non-MS population, no association was found between rs11099680 and the failure to control AHT. The results reveal a possible association between the rs11099680 RAAS polymorphism and uncontrolled AHT in MS-diagnosed patients. rs1040288 appears to be associated with uncontrolled blood pressure regardless of MS profile.

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Section: Discussionsupporting

confidence: 61%

Section: Introductionmentioning

confidence: 99%

Inefficient arterial hypertension control in patients with metabolic syndrome and its link to renin–angiotensin–aldosterone system polymorphisms

Morales-Suárez-Varela

Mansego

Vicedo‐Cabrera

et al. 2011

Hypertens Res

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“…captopril, has been reported in the literature. Likely, ACE polymorphism is involved here [15,16]. Others have suggested differences in drug metabolizing enzymes [17].…”

Section: Discussionmentioning

confidence: 91%

Inhibitory Efficacy and Biological Variability of Tryptophan Containing Dipeptides on Human Plasma Angiotensin Converting Enzyme Activity

Martin¹

2015

J Hypertens

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Background: Hypertension remains a major unsolved health problem with life threatening consequences. A potential innovative prophylactic approach against its development may be supplementation of daily food with natural antihypertensive compounds. In our work we tested the efficacy of novel tryptophan containing dipeptides from whey protein with respect to their inhibitory potency on the angiotensin converting enzyme (ACE) as well as their stability in human plasma. Methods: ACE activity from rabbit lung and human plasma as well as recombinant human ACE activity were measured using benzoyl-glycyl-histidyl-leucine as a substrate. Product formation of hippuric acid and histidyl-leucine was assessed by UV-HPLC. The stability of the peptides was quantified in human plasma and, in case of incubation with recombinant human angiotensin converting enzyme, in buffer. Variability of ACE inhibiting activity of peptides was assessed via analysis of coefficient of variation with particular reference to true inter-individual variability corrected for methodological and analytical errors. Results: Isoleucine-tryptophan (IW) had a stronger ACE inhibiting potency (IC 50 of 1.9 and 38.8 µmol/l with rabbit lung and human plasma ACE, respectively) than other tested peptides, i.e. glutamic acid-tryptophan (EW), tryptophanleucine (WL) and tryptophan-glutamic acid (WE). However, stability of IW showed a high degree of variability in plasma of different volunteers. In contrast EW, WL, WE were relatively stable in plasma and no major inter-individual variability was observed. Inhibition of plasma proteases extended plasma half-life of IW significantly. ACE did not contribute to peptide elimination. Conclusion: Milk whey protein represents a valuable source for bioactive peptides with ACE inhibitory potency that can be used as a food supplement to prevent, or in combination with other pharmaceutical agents to treat hypertension. However, in addition to the ACE inhibitory efficacy the stability of these peptides must be considered for in vivo ACE inhibition.

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“…Among recent studies of RAS genes for association with hypertension, 3 , 4 , 16 , 30 rs6682082 has been under consideration in a single study, in which no association was found therewith and uncontrolled arterial hypertension in an ethnic Spanish group. 30 In 2011, Song, et al 3 identified RAS-related genes that were associated with BP in the Korea Association Resource subject pool. They analyzed correlations between BP and 12 REN SNPs ( rs6679960 , rs4951307 , rs3737656 , rs1997034 , rs11571093 , rs2887284 , rs2368564 , rs11571082 , rs11571103 , rs10900555 , rs6693954, and rs16853059 ), which showed no association.…”

Section: Discussionmentioning

confidence: 99%

A Polymorphism of the Renin Geners6682082Is Associated with Essential Hypertension Risk and Blood Pressure Levels in Korean Women

et al. 2015

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PurposeThe aim of the present study was to investigate associations between the renin gene (REN) and the risk of essential hypertension and blood pressure (BP) levels in Koreans.Materials and MethodsTo outline the functional role of a single nucleotide polymorphism in the transcription of the REN gene, we conducted a case-control study of 1975 individuals: 646 hypertension (HT) patients and 1329 ethnically and age-matched normotensive subjects.ResultsLogistic regression analysis indicated that the genotypes AA/AG were strongly associated with risk of HT (odds ratio, 1.493; 95% confidence interval, 1.069-2.086, p=0.018) in female subjects. The genotypes AA/AG also showed significant association with higher blood pressure levels, both systolic and diastolic, in postmenopausal HT women (p=0.003 and p=0.017, respectively). Analysis of the promoter containing rs6682082 revealed a 2.4±0.01-fold higher activity in the A variant promoter than the G variant promoter, suggesting that rs6682082 is itself a functional variant.ConclusionWe suggest that the A allele of rs6682082 is a positive genetic marker for predisposition to essential hypertension and high BP in Korean women and may be mediated through the transcriptional activation of REN.

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How ineffective hypertension control in subjects treated with angiotensin-converting enzyme inhibitors is related to polymorphisms in the renin-angiotensin-aldosterone system

Cited by 7 publications

References 35 publications

Inefficient arterial hypertension control in patients with metabolic syndrome and its link to renin–angiotensin–aldosterone system polymorphisms

Inefficient arterial hypertension control in patients with metabolic syndrome and its link to renin–angiotensin–aldosterone system polymorphisms

Inhibitory Efficacy and Biological Variability of Tryptophan Containing Dipeptides on Human Plasma Angiotensin Converting Enzyme Activity

A Polymorphism of the Renin Geners6682082Is Associated with Essential Hypertension Risk and Blood Pressure Levels in Korean Women

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