Variable Number of Tandem Repeat of the 5'-Flanking Region of Type-C Human Natriuretic Peptide Receptor Gene Influences Blood Pressure Levels in Obesity-Associated Hypertension

Aoi, Noriko; Soma, Masayoshi; Nakayama, Tomohiro; Rahmutula, Dolkun; Kosuge, Kotoko; Izumi, Yasukatsu; Matsumoto, Koichí

doi:10.1291/hypres.27.711

Cited by 33 publications

(31 citation statements)

References 26 publications

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“…It is also known that pulse pressure is not only the indicator of arterial stiffness but also, influenced by peak systolic BP (30). Some of the genes found for pulse pressure are known to be associated with BP variation (31)(32)(33). However, adjustment for BP and excluding SNPs with suggestive association with systolic BP did not change the associations.…”

Section: Discussionmentioning

confidence: 98%

Arterial Stiffness and Decline in Kidney Function

Sedaghat¹,

Mattace-Raso²,

Hoorn³

et al. 2015

Clinical Journal of the American Society of Nephrology

135

112

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Background and objectives The independent link between arterial stiffness and CKD remains unknown. We investigated the association of indicators of arterial stiffness with decline in kidney function.Design, setting, participants, & measurements We studied 3666 participants (mean age =65 years old; 58% women) from the Rotterdam Study. Pulse pressure (PP), carotid stiffness, and pulse wave velocity (PWV) were measured. We created genetic risk scores for PP and PWV. Annual declines in kidney function and incident CKD were assessed using eGFR. To put our findings in context of the literature, we performed a meta-analysis of the available population-based studies.Results After a median (interquartile range) follow-up time of 11 (10.7-11.3) years, 601 participants with incident CKD were recognized. In the model adjusted for age, sex, mean arterial pressure, heart rate, and baseline GFR, each SD higher PP was associated with 0.15-ml/min per 1.73 m 2 steeper annual eGFR decline (95% confidence interval [95% CI], 0.10 to 0.20) and 11% higher risk of incident CKD (95% CI, 1.05 to 1.18). Each SD greater carotid stiffness was associated with 0.08-ml/min per 1.73 m 2 steeper annual eGFR decline (95% CI, 0.04 to 0.13) and 13% higher risk of incident CKD (95% CI, 1.05 to 1.22). Each SD higher PWV was associated with 7% higher risk of incident CKD (95% CI, 1.00 to 1.14). Incorporating our findings in a meta-analysis, each SD higher PP and PWV were associated with 16% (95% CI, 1.12 to 1.21) and 8% (95% CI, 1.03 to 1.14) higher risks of incident CKD. Each SD higher PP genetic risk score was associated with 0.06-ml/min per 1.73 m 2 steeper annual eGFR decline (95% CI, 0.01 to 0.10) and 8% higher risk of incident CKD (95% CI, 1.03 to 1.14). There was no association between PWV genetic risk score and kidney function decline.Conclusions Higher indices of arterial stiffness are associated with steeper decline in kidney function. This suggests that vascular stiffness could be considered as a target for delaying decline in kidney function.

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Section: Discussionmentioning

confidence: 98%

Arterial Stiffness and Decline in Kidney Function

Sedaghat¹,

Mattace-Raso²,

Hoorn³

et al. 2015

Clinical Journal of the American Society of Nephrology

135

112

View full text Add to dashboard Cite

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“…Both groups were recruited from the Tokyo area in Japan. Informed consent was obtained from each subject according to a protocol approved by the Human Studies Committee of Nihon University (17).…”

Section: Subjectsmentioning

confidence: 99%

“…The clinical laboratory of our university hospital measured the total cholesterol and the high-density lipoprotein (HDL) cholesterol concentrations in the plasma, as well as the creatinine and uric acid concentrations in the serum (15,17,18).…”

Section: Biochemical Analysismentioning

confidence: 99%

A Haplotype-Based Case-Control Study Examining Human Extracellular Superoxide Dismutase Gene and Essential Hypertension

et al. 2008

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It has been reported that oxidative stress is involved in the pathophysiology of essential hypertension (EH),which is a multifactorial disorder. Extracellular superoxide dismutase (EC-SOD) protects the human body from oxidative stress by converting the toxic superoxide anion (O2 -) into less toxic hydrogen peroxide (H2O2). In EC-SOD knockout mice, blood pressure was reported to be significantly higher than that seen in wild-type mice. The aim of this study was thus to investigate the relationship between EH and the human EC-SOD gene by using single-nucleotide polymorphisms (SNPs) in a haplotype-based case-control study.We selected 6 SNPs within the human EC-SOD gene (rs13306703, rs699473, rs699474, rs17881426, rs2536512 and rs1799895), and then performed case-control studies in 243 EH patients and 251 age-matched normotensive (NT) subjects. In Japanese subjects, no heterogeneity was found for rs699474, and no significant differences were observed between the EH and NT groups for the overall distribution of the genotypes or the alleles for each of the SNPs. However, in the haplotype-based case-control study that used rs13306703 and rs2536512, significant differences were observed in the overall distribution (

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“…Although no significant difference in the overall frequency of this variable number of tandem repeat (VNTR) was found between the normotension and essential hypertension groups, the blood pressure level of the essential hypertensive patients with the 5/6 genotype was significantly higher in obese subjects. This suggests that the VNTR of the 5'-flanking region of the NPRC gene influences blood pressure levels in obesity-associated hypertension [45]. Unanalyzed regions should be targeted for future molecular studies.…”

Section: Natriuretic Peptide Receptorsmentioning

confidence: 99%

The Genetic Contribution of the Natriuretic Peptide System to Cardiovascular Diseases

Nakayama

2005

Endocr J

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Abstract. Three types of natriuretic peptides (NP) have been isolated: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP). The NP family elicits a number of vascular, renal and endocrine effects that help to maintain blood pressure and extracellular fluid volume. These effects are mediated by the specific binding of NP to cell surface receptors that have been characterized, purified and cloned from cells of the vasculature, kidney, adrenal gland and brain. There are 3 subtypes of NP receptors: type A natriuretic peptide receptor (NPRA), type B natriuretic peptide receptor (NPRB), and type C natriuretic peptide receptor (NPRC). All 3 subtypes affect cellular second messenger activity. NPRA and NPRB are guanylyl cyclase receptors, and their activation increases cGMP levels. Activation of NPRC results in inhibition of adenylyl cyclase activity. Human NPRA has a high structural homology with human NPRB, and contains a highly-conserved guanylyl cyclase domain. ANP and BNP bind primarily to NPRA, which is found in the vasculature, causing vasodilation and inhibition of vascular smooth muscle cell proliferation. The present paper contains a review of NPs and their receptors and the genetic contribution of the NP system to cardiovascular diseases such as essential hypertension and myocardial infarction.

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Variable Number of Tandem Repeat of the 5'-Flanking Region of Type-C Human Natriuretic Peptide Receptor Gene Influences Blood Pressure Levels in Obesity-Associated Hypertension

Cited by 33 publications

References 26 publications

Arterial Stiffness and Decline in Kidney Function

Arterial Stiffness and Decline in Kidney Function

A Haplotype-Based Case-Control Study Examining Human Extracellular Superoxide Dismutase Gene and Essential Hypertension

The Genetic Contribution of the Natriuretic Peptide System to Cardiovascular Diseases

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