Oxidative stress contributes to vascular endothelial dysfunction in heart failure

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Abstract

Congestive heart failure (HF) is characterized by inadequate nitric oxide (NO) production in the vasculature. Because NO is degraded by oxygen radicals, we hypothesized that NO is degraded faster in HF from inadequate peripheral arterial antioxidant reserves. HF was induced in male Sprague-Dawley rats by left coronary artery ligation. Vascular endothelial function was evaluated by measuring the NO-mediated vasorelaxation response to acetylcholine (ACh; 10-9-10-4 M) in excised aortas. This was repeated with the free radical generator pyrogallol (20μM) and again with pyrogallol and superoxide dismutase (SOD; 60U/ml). Aortic and myocardial SOD activity was also determined. ACh-induced vasorelaxation was reduced in HF (n=9) compared with normal control rats (n=11; P<0.001). Pyrogallol further reduced vasorelaxation in HF: 74±11% at 10-4 M ACh versus 58 ± 10% in normal control rats (P<0.004). There was a trend (P=0.06) toward reduced SOD activity in HF aortas. In conclusion, altered NO-dependent vasorelaxation in HF is in part due to excessive degradation of NO and is likely related to reduced vascular SOD activity.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume281
Issue number4 50-4
StatePublished - 2001

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Blood Vessels
Oxidative Stress
Heart Failure
Nitric Oxide
Pyrogallol
Vasodilation
Aorta
Acetylcholine
Superoxide Dismutase
Free Radicals
Ligation
Sprague Dawley Rats
Reactive Oxygen Species
Coronary Vessels
Antioxidants

Keywords

  • Congestive heart failure
  • Endothelial function
  • Nitric oxide
  • Superoxide dismutase

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Oxidative stress contributes to vascular endothelial dysfunction in heart failure",
abstract = "Congestive heart failure (HF) is characterized by inadequate nitric oxide (NO) production in the vasculature. Because NO is degraded by oxygen radicals, we hypothesized that NO is degraded faster in HF from inadequate peripheral arterial antioxidant reserves. HF was induced in male Sprague-Dawley rats by left coronary artery ligation. Vascular endothelial function was evaluated by measuring the NO-mediated vasorelaxation response to acetylcholine (ACh; 10-9-10-4 M) in excised aortas. This was repeated with the free radical generator pyrogallol (20μM) and again with pyrogallol and superoxide dismutase (SOD; 60U/ml). Aortic and myocardial SOD activity was also determined. ACh-induced vasorelaxation was reduced in HF (n=9) compared with normal control rats (n=11; P<0.001). Pyrogallol further reduced vasorelaxation in HF: 74±11{\%} at 10-4 M ACh versus 58 ± 10{\%} in normal control rats (P<0.004). There was a trend (P=0.06) toward reduced SOD activity in HF aortas. In conclusion, altered NO-dependent vasorelaxation in HF is in part due to excessive degradation of NO and is likely related to reduced vascular SOD activity.",
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T1 - Oxidative stress contributes to vascular endothelial dysfunction in heart failure

AU - Indik, Julia H

AU - Goldman, Steven

AU - Gaballa, M. A.

PY - 2001

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N2 - Congestive heart failure (HF) is characterized by inadequate nitric oxide (NO) production in the vasculature. Because NO is degraded by oxygen radicals, we hypothesized that NO is degraded faster in HF from inadequate peripheral arterial antioxidant reserves. HF was induced in male Sprague-Dawley rats by left coronary artery ligation. Vascular endothelial function was evaluated by measuring the NO-mediated vasorelaxation response to acetylcholine (ACh; 10-9-10-4 M) in excised aortas. This was repeated with the free radical generator pyrogallol (20μM) and again with pyrogallol and superoxide dismutase (SOD; 60U/ml). Aortic and myocardial SOD activity was also determined. ACh-induced vasorelaxation was reduced in HF (n=9) compared with normal control rats (n=11; P<0.001). Pyrogallol further reduced vasorelaxation in HF: 74±11% at 10-4 M ACh versus 58 ± 10% in normal control rats (P<0.004). There was a trend (P=0.06) toward reduced SOD activity in HF aortas. In conclusion, altered NO-dependent vasorelaxation in HF is in part due to excessive degradation of NO and is likely related to reduced vascular SOD activity.

AB - Congestive heart failure (HF) is characterized by inadequate nitric oxide (NO) production in the vasculature. Because NO is degraded by oxygen radicals, we hypothesized that NO is degraded faster in HF from inadequate peripheral arterial antioxidant reserves. HF was induced in male Sprague-Dawley rats by left coronary artery ligation. Vascular endothelial function was evaluated by measuring the NO-mediated vasorelaxation response to acetylcholine (ACh; 10-9-10-4 M) in excised aortas. This was repeated with the free radical generator pyrogallol (20μM) and again with pyrogallol and superoxide dismutase (SOD; 60U/ml). Aortic and myocardial SOD activity was also determined. ACh-induced vasorelaxation was reduced in HF (n=9) compared with normal control rats (n=11; P<0.001). Pyrogallol further reduced vasorelaxation in HF: 74±11% at 10-4 M ACh versus 58 ± 10% in normal control rats (P<0.004). There was a trend (P=0.06) toward reduced SOD activity in HF aortas. In conclusion, altered NO-dependent vasorelaxation in HF is in part due to excessive degradation of NO and is likely related to reduced vascular SOD activity.

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KW - Endothelial function

KW - Nitric oxide

KW - Superoxide dismutase

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