Aldosterone Antagonism Improves Endothelial-Dependent Vasorelaxation in Heart Failure via Upregulation of Endothelial Nitric Oxide Synthase Production
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Accession number;06A0306325
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| Title;Aldosterone Antagonism Improves Endothelial-Dependent Vasorelaxation in Heart Failure via Upregulation of Endothelial Nitric Oxide Synthase Production |
| Author;
THAI HOANG M.
(From The Section Of Cardiology, Dep. Of Medicine, Southern Arizona Va Health Care System, Sarver Heart Center, Univ. ...)
DO BAO Q.
(From The Section Of Cardiology, Dep. Of Medicine, Southern Arizona Va Health Care System, Sarver Heart Center, Univ. ...)
TRAN TRUNG D.
(From The Section Of Cardiology, Dep. Of Medicine, Southern Arizona Va Health Care System, Sarver Heart Center, Univ. ...)
GABALLA MOHAMED A.
(From The Section Of Cardiology, Dep. Of Medicine, Southern Arizona Va Health Care System, Sarver Heart Center, Univ. ...)
GOLDMAN STEVEN
(From The Section Of Cardiology, Dep. Of Medicine, Southern Arizona Va Health Care System, Sarver Heart Center, Univ. ...)
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Journal Title;J Card Fail
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Journal Code:W1342A
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ISSN:1071-9164
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VOL.12;NO.3;PAGE.240-245(2006)
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| Figure&Table&Reference;FIG.2, TBL.2, REF.46 |
| Pub. Country;United States |
| Language;English |
| Abstract;Altering the renin-angiotensin aldosterone system improve mortality in heart failure (HF) in part through an improvement in nitric oxide (NO)-mediated endothelial function. This study examined if spironolactone affects endothelial nitric oxide synthase (eNOS) and NO-mediated vasorelaxation in HF. Rats with HF after coronary artery ligation were treated with spironolactone for 4 weeks. Rats with HF had a decrease (P < .05) in left ventricular (LV) systolic pressure (130 .+-. 7 versus 118 .+-. 6 mm Hg) and LV pressure with respect to time (9122 .+-. 876 versus 4500 .+-. 1971 mm Hg/second) with an increase in LV end-diastolic pressure (4 .+-. 2 versus 23 .+-. 8 mm Hg). Spironolactone did not affect hemodynamics but it improved (P < .05) endothelial-dependent vasorelaxation at more than 10'-8' M acetylcholine that was abolished with N'G'-monomethyl-L-arginine. The eNOS levels were decreased (P < .05) in the LV and the aorta; spironolactone restored LV and aortic eNOs levels to normal. Spironolactone prevents the decrease in eNOS in the LV and aorta and improves NO-dependent vasorelaxation, suggesting that one potential mechanism of spironolactone is an improvement in vasoreactivity mediated though an increase in NO. Copyright 2006 Elsevier B.V., Amsterdam.All rights reserved. |
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