Journals / Düzce Tıp Fakültesi Dergisi / 2005 / Cilt: 7 - Sayı: 2

Asymmetrıcal Dımethylargınıne (ADMA)

Asimetrik Dimetilarginin (ADMA)

Pages
36–41
Publication Date
2005-07-01
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Recently, it was found that ADMA was significantly elevated in animals and humans with hypercholesterolemia.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Asymmetric dimethylarginine (ADMA) is the principal endogenous inhibitor of nitric oxide synthase.
📊
Key Findings & Data:It regulates rates of nitric oxide (NO) formation.
💡
Conclusion & Impact:Recently, it was found that ADMA was significantly elevated in animals and humans with hypercholesterolemia.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Asimetrik dimetilarginin · Nitrik oksit · Endotel disfonksiyonu

Abstract

Asymmetric dimethylarginine (ADMA) is the principal endogenous inhibitor of nitric oxide synthase. It regulates rates of nitric oxide (NO) formation. There is abundant evidence that the endothelium plays a crucial role in the maintenance of vascular tone and structure. One of the major endothelium-derived vasoactive mediators is nitric oxide , which has been characterized as an "endogenous anti-atherosclerotic molecule". Thus, ADMA might be thought as a key role contributing to endothelial dysfunction. Recently, it was found that ADMA was significantly elevated in animals and humans with hypercholesterolemia. ADMA also participated in inflammatory reaction in atherosclerosis. Elevated plasma concentrations of ADMA are also present in hypercholesterolemic and hypertensive patients, in patients with chronic heart failure, and in other patient groups at high risk of developing cardiovascular disease. Elevation of ADMA induces dysfunction of the endothelium, which becomes clinically evident by impaired endothelium-dependent vasodilation, hyperaggregability of platelets, and enhanced monocyte adhesion. Recent prospective studies suggest that endothelial dysfunction indicates an increased risk of future cardiovascular events. Most of scientifics found that ADMA is a novel cardiovascular risk factor. Plasma ADMA is now available as a routine laboratory evaluation

Özet

Asimetrik dimetilarginin (ADMA), esas olarak endojen nitrik oksit sentaz inhibitörüdür. ADMA, nitrik oksit oluşum hızını düzenler. Vasküler tonus ve yapısının sürdürülmesinde temel rolü oynadığına dair çok miktarda kanıt bulunmaktadır. ‘Endojen anti-aterosklerotik molekül’ olarak bilinen nitrik oksit, major endotel kaynaklı vazoaktif mediatörüdür. Dolayısıyla ADMA’nın endotel disfonksiyonu ile ilgili anahtar rolü oynayabileceği düşünülmektedir. Son zamanlarda, ADMA hiperkolesterolemili insanlar ve hayvanlarda önemli oranda yüksek bulunmuştur. ADMA aterosklerozun inflamatuvar reaksiyon sürecine de katılmaktadır. ADMA plazma konsantrasyonları olan hasta grubunda kronik kalp yetmezliği ve diğer kardiyovasküler hastalıkların yanısıra hiperkolesterolemili ve hipertansif hastalarda da artmaktadır. Bozulan endotel bağımlı vazodilatasyon, plateletlerin agregabilite artışı ve monosit adezyonu artışının klinik delili olarak ortaya çıkan endotel disfonksiyonu, ADMA artışını uyarır. Son prospektif çalışmalar, ortaya çıkabilecek kardiyovasküler olayların endotel disfonksiyonunu desteklemektedir. Birçok bilim adamı ADMA’yı yeni bir kardiyovasküler risk faktörü olarak düşünmektedir. Günümüzde plazma ADMA’nın rutin laboratuvarlarda ölçümü mümkündür

🔖

Cite This Article

BUĞDAYCI, G., SERİN, E. (2005). Asymmetrıcal Dımethylargınıne (ADMA). Düzce Tıp Fakültesi Dergisi, Cilt: 7 - Sayı: 2, 36–41. https://ajindex.com/articles/420330

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (13)

  1. Mugge A, Hanefeld C, Boger RH: Plasma concentration of asymmetric dimethylarginine and the risk of coronary heart disease: rationale and design of the multicenter CARDIAC study. Atheroscler Suppl. 4: 29-32, 2003.
  2. Lenzen H, Tsikas D, Boger RH: Asymmetric dimethylarginine ( ADMA ) and the risk for coronary heart disease: the multicenter CARDIAC study. Eur J Clin Pharmacol. 8:1-5, 2005.
  3. Leiper JM, Vallance P: The synthesis and metabolism of asymmetric dimethylarginine (ADMA). Eur J Clin Pharamacol. 8: 1-6, 2005. Cooke JP: Does ADMA cause endothelial dysfunction? Arterioscler Thromb Vasc Biol. 20: 2032-37, 2000.
  4. Jiang J, Tang Y, Li N, Deng H, Li Y: Effect of simvastatin on endothelium-dependent vasorelaxation and endogenous nitric oxide synthase inhibitor. Acta Pharmacol. 25: 893- 901, 2004. Sela BA: ADMA (Asymmetric dimethylarginine) the inhibitor of nitric oxide (NO) Snythesis: a new marker for vascular pathology. Harefuah. 144: 655-9, 2005.
  5. Endemann DH, Schiffrin E: Endothelial Dysfunction. J Am Soc. Nephrol. 15:1983-92, 2004.
  6. Miyazaki H, Matsuoka H, Cooke JP: Endogenous nitric oxide synthase inhibitor: a novel marker of atherosclerosis. Circulation. 99: 1141-46, 1999.
  7. Gornik HL, Creager MA: Arginine, endothelial and vascular health. J of Nutr. 134: 2880S-87S, 2004.
  8. Chauhan A, More RS, Mullins PA: Aging- associated endothelial dysfunction in humans is reversed by L-Arginine. J Am Coll Cardiol. 28: 1796-1804, 1996. Celermajer DS: Endothelial dysfunction: does it matter? Is it reversible? J Am Cardiol. 30: 325-333, 1997.
  9. Achan V, Ho HK, Heeschen C, Stuehlinger M, Jang JJ, Kimoto M, Vallance P, Cooke JP: ADMA regulates angiogenesis genetic and metabolic evidence. Vasc Med. 10: 7-14, 2005.
  10. Stühlinger M, Abbasi F, Chu JW, Lamendola C, McLaughlin TL, Cooke JP, Reaven GM, Tsao PS: Relationship between insulin resistance and an endogenous nitric oxide synthase inhibitor. J Am.Med.Assoc. 287:1420-26,2002.
  11. Lentz SR, Rodionow RN, Dayol S: Hyperhomocysteinemia, endothelial dysfunction and cardiovascular risk: the potential role of ADMA. Atherosclerosis Suppl. 4: 61-5, 2003. Boger RH: Association of asymmetric dimethylarginine and endothelial dysfunction. Clin Chem Lab Med. 41: 1467-72, 2003.
  12. Holven KB, Haugstad TS, Holm T, Aurust P, Ose L, Nenseter MS: Folic acid treatment reduces elevated plasma levels of asymmetric dimethylarginine in hyperhomocysteinaemic subjects. Br J Nutr. 89:359-63, 2003.
  13. Sydow K, Schwedhelm E, Arakawa N, Bode- Boger SM, Tsikas D, Hornig B