Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2019 Jul 22;17(3):613-620.
doi: 10.5114/aoms.2019.86770. eCollection 2021.

The association of endothelin-1 gene polymorphism and its plasma levels with hypertension and coronary atherosclerosis

Affiliations

The association of endothelin-1 gene polymorphism and its plasma levels with hypertension and coronary atherosclerosis

Nazanin Ebrahimi et al. Arch Med Sci. .

Abstract

Introduction: Endothelin-1 (ET-1) is the most potent among all vasoconstrictors, and its association with cardiovascular diseases has been reported before. Our aim was to investigate the association of ET-1 plasma level and its gene polymorphisms (rs5370 and rs10478694) with hypertension and coronary atherosclerosis (CA).

Material and methods: This study was carried out on 128 women and 132 men, who were divided into 4 groups: hypertensive without atherosclerosis (H+A-); hypertensive with atherosclerosis (H+A+); non-hypertensive with atherosclerosis (H-A+); and non-hypertensive without atherosclerosis (control group). Endothelin-1 plasma levels were measured by ELISA, and gene polymorphisms were detected by polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) methods. Coronary artery diseases (CAD) were then defined based on angiography data.

Results: The ET-1 plasma level was significantly higher in the H+A+ group in comparison with the other groups, especially H+A-. Comparing people with CA and those without it, the highest frequency level of the T allele of rs5370 was found in people with CA. Significantly higher frequencies of the 3A allele were detected in hypertensive patients in comparison with non-hypertensive individuals, when analyzing rs10478694.

Conclusions: Endothelin-1 plasma level shows a direct association with the risk of CA development. The T allele of rs5370 can be regarded as a risk factor for CA development. The 3A allele of rs10478694 can be associated with the risk of hypertension; therefore, it can be concluded that ET-1 and its gene polymorphisms play an important role in CA development and hypertension observed in the south-eastern populations of Iran.

Keywords: SNP; atherosclerosis; endothelin-1; hypertension; rs1046872; rs5370.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Comparison of endothelin-1 plasma level among the four groups under investigation Endothelin-1 plasma level in the H+A+ group is significantly higher than in the other groups (p = 0.018). Only the difference of endothelin-1 plasma level observed between H+A+ and H+A– is significant (p = 0.017). H+A– – hypertension and no coronary artery disease, H–A+ – coronary artery disease and no hypertension, H+A+ – coronary artery disease and hypertension, H–A– – no coronary artery disease and no hypertension. Significant difference at < 0.05

Similar articles

Cited by

References

    1. Maguire JJ, Davenport AP. Endothelin receptors and their antagonists. Semin Nephrol. 2015;3:125–36. - PMC - PubMed
    1. Peto H, Corder R, Janes RW, Wallace BA. A molecular model for human Big-Endothelin-1 (Big ET-1) FEBS Lett. 1996;394:191–5. - PubMed
    1. Schiffrin EL. Vascular endothelin in hypertension. Vascul Pharmacol. 2005;43:19–29. - PubMed
    1. Forouzanfar MH, Liu P, Roth GA, et al. Global burden of hypertension and systolic blood pressure of at least 110 to 115 mm Hg, 1990-2015. JAMA. 2017;317:165–82. - PubMed
    1. Pusuroglu H, Akgul O, Erturk M, et al. Red cell distribution width and end-organ damage in patients with systo-diastolic hypertension. Arch Med Sci. 2016;12:319–25. - PMC - PubMed