2009
DOI: 10.1038/jhh.2009.19
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An association between resistant hypertension and the null GSTM1 genotype

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Cited by 15 publications
(13 citation statements)
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“…Some studies estimate that other members of the GST enzyme family must have compensated for the absence of a functional enzyme in the double deletion subjects [33,34], which leads to the same level of activity of GST both in the null and active genotype. In addition to not con rming our initial hypothesis, our results may also not support the hypothesis that expression of the GSTM1 gene could protect against resistant hypertension [11].…”
Section: Discussioncontrasting
confidence: 95%
See 1 more Smart Citation
“…Some studies estimate that other members of the GST enzyme family must have compensated for the absence of a functional enzyme in the double deletion subjects [33,34], which leads to the same level of activity of GST both in the null and active genotype. In addition to not con rming our initial hypothesis, our results may also not support the hypothesis that expression of the GSTM1 gene could protect against resistant hypertension [11].…”
Section: Discussioncontrasting
confidence: 95%
“…These results suggest that GST could affect the bioavailability of certain drugs which acts as GST enzyme substrate. To date, no study to our knowledge has evaluated the link between GST and antihypertensive responses, although Glutathione S-transferases Mu1 deletion has been associated with resistant hypertension [11]. In this study we hypothesized that the active variants of Glutathione S-transferases Mu1 (GSTM1) and theta 1 (GSTT1) which have normal detoxi cation activity could reduce the bioavailability of certain antihypertensive drugs and therefore affect the control of BP in hypertensive patients.…”
Section: Introductionmentioning
confidence: 99%
“…Recent reviews targeting strategies to uncover the genetic background of complex traits (such as hypertension) have suggested that extreme phenotype samples (such as TRH) may be enriched for variants underlying the disease 26,27 . Several small candidate gene studies have reported associations with TRH that warrant follow‐up investigations 28–30 . For instance, one study reported the angiotensinogen M235T polymorphism was associated with increased risk for TRH, especially after age 50, highlighting a potential gene variant by age interaction 29 .…”
Section: Discussionmentioning
confidence: 99%
“…26,27 Several small candidate gene studies have reported associations with TRH that warrant follow-up investigations. [28][29][30] For instance, one study reported the angiotensinogen M235T polymorphism was associated with increased risk for TRH, especially after age 50, highlighting a potential gene variant by age interaction. 29 Replication of preliminary results from smaller studies should be carried out in larger cohorts.…”
Section: Discussionmentioning
confidence: 99%
“…Decrease GSTM1 expression may reduce antioxidant defenses, resulting low GSTM1 levels may lead to increased superoxide formation and reduced nitric oxide bioavailability [37]. Endothelial dysfunction is defined as the imbalance between the production and bioavailability of endothelium-derived relaxing factors (EDRFs) and endothelium derived contractile factors (EDCFs), associated with increased bioavailability of oxygen reactive species (ROS) and decreased antioxidant capacity characterized as oxidative stress [38].…”
Section: Discussionmentioning
confidence: 99%