Decreased activity of the L-arginine-nitric oxide metabolic pathway in patients with congestive heart failure.

Abstract:

BACKGROUND:Impaired endothelium-dependent, nitric oxide (NO)-mediated vasodilation may contribute to increased vasomotor tone in patients with heart failure. Whether decreased endothelium-dependent, NO-mediated vasodilation in patients with heart failure is due to decreased synthesis or increased degradation of NO is unknown. METHODS AND RESULTS:To specifically assess the synthetic activity of the L-arginine-NO metabolic pathway, urinary excretion of [15N]nitrates and [15N]urea was determined after a primed continuous intravenous infusion of L-[15N]arginine (40 micromol/kg) in 16 patients with congestive heart failure and 9 age-matched normal control subjects at rest and during submaximal treadmill exercise. After infusion of L-[15N]arginine, 24-hour urinary excretion of [15N]nitrates was decreased in patients with congestive heart failure at rest (2.2+/-0.5 versus 8.0+/-2.3 micromol/24 h) and during submaximal exercise (2.4+/-1.2 versus 11. 4+/-4.0 micromol/24 h) compared with control subjects (both P<0.01). After infusion of L-[15N]arginine, 24-hour urinary excretions of [15N]urea at rest in patients with congestive heart failure and control subjects were not different (1.1+/-0.3 versus 1.2+/-0.2 mmol/24 h, P>0.20). CONCLUSIONS:A specific decrease in synthetic activity of the L-arginine-NO metabolic pathway contributes to decreased endothelium-dependent vasodilation in patients with congestive heart failure.

journal_name

Circulation

journal_title

Circulation

authors

Katz SD,Khan T,Zeballos GA,Mathew L,Potharlanka P,Knecht M,Whelan J

doi

10.1161/01.cir.99.16.2113

subject

Has Abstract

pub_date

1999-04-27 00:00:00

pages

2113-7

issue

16

eissn

0009-7322

issn

1524-4539

journal_volume

99

pub_type

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