Anjiotensin dönüştürücü enzim ve I/D polimorfizmi

Volume: 12 Number: 4 April 16, 2009
  • Sebahat Turgut

Anjiotensin dönüştürücü enzim ve I/D polimorfizmi

Abstract

SüleymanDemirel Üniversitesi TIP FAKÜLTESİ DERGİSİ: 2005 Aralık; 12(4) Anjiotensin dönüştürücü enzim ve I/D polimorfizmi Sebahat Turgut Özet Renin-anjiotensin sisteminin kardiovasküler hastalıkların patogenezinde rolü bulunmaktadır ve kalp yetmezliği ile hipertansiyon tedavisinde kullanılan anjiotensin dönüştürücü enzim (ADE) inhibitörleri kardiovasküler sistemde ADE'nin önemli rolünü vurgulamaktadır. Bu yazı ile ADE ve I/D polimorfizmi bilgileri derlenmiştir. ADE, anjiotensin I'i kuvvetli bir vazokonstriktör olan anjiotensin II'e dönüştürür ve bradikininin etkinliğini azaltır. ADE geni insan 17.kromozomunda intron 16'da üç genotip olarak eksprese olur. Bu genotipler “insertion” ve “deletion” olarak isimlendirilen I ve D alelleridir. D aleli, koroner kalp hastalığı ve ventriküler hipertrofi gibi birçok patolojik durumun gelişme riskinde artışla ilişkilidir. D alelli homozigot kişiler birçok kardiak durumda kötü bir prognoza sahiptir. I aleli ise sporcularda dayanıklılık performanslarında artış ile ilişkilidir. Anahtar kelimeler: Anjiotensin dönüştürücü enzim, ADE I/D polimorfizmi, kardiovasküler hastalıklar Abstract Angiotensin Converting Enzyme and I/D Polymorphism The renin-angiotensin system plays a role in the pathogenesis of cardiovascular diseases and the efficacy of angiotensin converting enzyme (ACE) inhibitors in the treatment of hypertension and heart failure emphasize the prominent role of ACE in the cardiovascular system. This review aims to discuss angiotensin converting enzyme and I/D polymorphism. ACE converts angiotensin I to the potent vasoconstrictor angiotensin II and that degrades bradykinin. ACE gene is located on human chromosome 17 expressing three genotypes within the intron 16 of the related gene structure. These genotypes are classified as I and D alleles which are termed as insertion and deletion, respectively. The D allele has been associated with an increased risk of developing several pathological processes, such as coronary heart disease and ventricular hypertrophy. Several cardiac conditions appear to have a worse prognosis in subjects homozygous for the D allele, whereas the I allele has been associated with enhanced endurance performance in sportsmen. Key words: Angiotensin converting enzyme, ACE I/D polymorphism, cardiovascular diseases

Keywords

References

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Details

Primary Language

English

Subjects

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Journal Section

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Authors

Sebahat Turgut This is me

Publication Date

April 16, 2009

Submission Date

April 16, 2009

Acceptance Date

-

Published in Issue

Year 2005 Volume: 12 Number: 4

APA
Turgut, S. (2009). Anjiotensin dönüştürücü enzim ve I/D polimorfizmi. Medical Journal of Süleyman Demirel University, 12(4), 53-57. https://doi.org/10.17343/sdutfd.68335
AMA
1.Turgut S. Anjiotensin dönüştürücü enzim ve I/D polimorfizmi. Med J SDU. 2009;12(4):53-57. doi:10.17343/sdutfd.68335
Chicago
Turgut, Sebahat. 2009. “Anjiotensin Dönüştürücü Enzim Ve I D Polimorfizmi”. Medical Journal of Süleyman Demirel University 12 (4): 53-57. https://doi.org/10.17343/sdutfd.68335.
EndNote
Turgut S (April 1, 2009) Anjiotensin dönüştürücü enzim ve I/D polimorfizmi. Medical Journal of Süleyman Demirel University 12 4 53–57.
IEEE
[1]S. Turgut, “Anjiotensin dönüştürücü enzim ve I/D polimorfizmi”, Med J SDU, vol. 12, no. 4, pp. 53–57, Apr. 2009, doi: 10.17343/sdutfd.68335.
ISNAD
Turgut, Sebahat. “Anjiotensin Dönüştürücü Enzim Ve I D Polimorfizmi”. Medical Journal of Süleyman Demirel University 12/4 (April 1, 2009): 53-57. https://doi.org/10.17343/sdutfd.68335.
JAMA
1.Turgut S. Anjiotensin dönüştürücü enzim ve I/D polimorfizmi. Med J SDU. 2009;12:53–57.
MLA
Turgut, Sebahat. “Anjiotensin Dönüştürücü Enzim Ve I D Polimorfizmi”. Medical Journal of Süleyman Demirel University, vol. 12, no. 4, Apr. 2009, pp. 53-57, doi:10.17343/sdutfd.68335.
Vancouver
1.Sebahat Turgut. Anjiotensin dönüştürücü enzim ve I/D polimorfizmi. Med J SDU. 2009 Apr. 1;12(4):53-7. doi:10.17343/sdutfd.68335

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