Abstract
Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide-dependent vasodilation. In 113 patients with chronic heart failure (CHF) and 26 controls, ADMA level was studied in relation to peripheral blood flow and vasodilator capacity. Further, the effects of allopurinol on concentrations of reactive oxygen species (ROS) and ADMA and peripheral vasodilator capacity were tested in a double-blind design. ADMA level was found to be elevated in CHF patients as compared with controls and increased in parallel with New York Heart Association (NYHA) class and exercise capacity (all P 0.0001). The level of ADMA predicted resting blood flow (P 0.05) and postischemic vasodilator capacity (P 0.001). Sixty eight patients died during the follow-up period. The level of ADMA predicted survival after multivariable adjustment (P = 0.04). Allopurinol reduced uric acid (UA) concentration (P 0.001) and decreased ROS concentration (allantoin, P 0.01). Allopurinol lowered ADMA concentration (P = 0.02); postischemic vasodilation as well as endothelium-dependent vasodilation (both P 0.05) improved. ADMA may be a pathophysiologic factor that is modulated by ROS accumulation and contributes to impaired vascular regulation in CHF.
| Original language | English |
|---|---|
| Pages (from-to) | 506-512 |
| Number of pages | 7 |
| Journal | Clinical Pharmacology and Therapeutics |
| Volume | 88 |
| Issue number | 4 |
| DOIs | |
| Publication status | Published - Oct 2010 |
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ASJC Scopus subject areas
- Pharmacology
- Pharmacology (medical)
- Medicine(all)
Cite this
Elevated levels of asymmetric dimethylarginine in chronic heart failure : A Pathophysiologic link between oxygen radical load and impaired vasodilator capacity and the therapeutic effect of allopurinol. / Von Haehling, S.; Bode-Böger, S. M.; Martens-Lobenhoffer, J.; Rauchhaus, M.; Schefold, J. C.; Genth-Zotz, S.; Karhausen, T.; Cicoira, M.; Anker, S. D.; Doehner, W.
In: Clinical Pharmacology and Therapeutics, Vol. 88, No. 4, 10.2010, p. 506-512.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Elevated levels of asymmetric dimethylarginine in chronic heart failure
T2 - A Pathophysiologic link between oxygen radical load and impaired vasodilator capacity and the therapeutic effect of allopurinol
AU - Von Haehling, S.
AU - Bode-Böger, S. M.
AU - Martens-Lobenhoffer, J.
AU - Rauchhaus, M.
AU - Schefold, J. C.
AU - Genth-Zotz, S.
AU - Karhausen, T.
AU - Cicoira, M.
AU - Anker, S. D.
AU - Doehner, W.
PY - 2010/10
Y1 - 2010/10
N2 - Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide-dependent vasodilation. In 113 patients with chronic heart failure (CHF) and 26 controls, ADMA level was studied in relation to peripheral blood flow and vasodilator capacity. Further, the effects of allopurinol on concentrations of reactive oxygen species (ROS) and ADMA and peripheral vasodilator capacity were tested in a double-blind design. ADMA level was found to be elevated in CHF patients as compared with controls and increased in parallel with New York Heart Association (NYHA) class and exercise capacity (all P 0.0001). The level of ADMA predicted resting blood flow (P 0.05) and postischemic vasodilator capacity (P 0.001). Sixty eight patients died during the follow-up period. The level of ADMA predicted survival after multivariable adjustment (P = 0.04). Allopurinol reduced uric acid (UA) concentration (P 0.001) and decreased ROS concentration (allantoin, P 0.01). Allopurinol lowered ADMA concentration (P = 0.02); postischemic vasodilation as well as endothelium-dependent vasodilation (both P 0.05) improved. ADMA may be a pathophysiologic factor that is modulated by ROS accumulation and contributes to impaired vascular regulation in CHF.
AB - Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide-dependent vasodilation. In 113 patients with chronic heart failure (CHF) and 26 controls, ADMA level was studied in relation to peripheral blood flow and vasodilator capacity. Further, the effects of allopurinol on concentrations of reactive oxygen species (ROS) and ADMA and peripheral vasodilator capacity were tested in a double-blind design. ADMA level was found to be elevated in CHF patients as compared with controls and increased in parallel with New York Heart Association (NYHA) class and exercise capacity (all P 0.0001). The level of ADMA predicted resting blood flow (P 0.05) and postischemic vasodilator capacity (P 0.001). Sixty eight patients died during the follow-up period. The level of ADMA predicted survival after multivariable adjustment (P = 0.04). Allopurinol reduced uric acid (UA) concentration (P 0.001) and decreased ROS concentration (allantoin, P 0.01). Allopurinol lowered ADMA concentration (P = 0.02); postischemic vasodilation as well as endothelium-dependent vasodilation (both P 0.05) improved. ADMA may be a pathophysiologic factor that is modulated by ROS accumulation and contributes to impaired vascular regulation in CHF.
UR - http://www.scopus.com/inward/record.url?scp=77957021340&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77957021340&partnerID=8YFLogxK
U2 - 10.1038/clpt.2010.116
DO - 10.1038/clpt.2010.116
M3 - Article
C2 - 20827268
AN - SCOPUS:77957021340
VL - 88
SP - 506
EP - 512
JO - Clinical Pharmacology and Therapeutics
JF - Clinical Pharmacology and Therapeutics
SN - 0009-9236
IS - 4
ER -