Sd. Katz et al., Decreased activity of the L-arginine-nitric oxide metabolic pathway in patients with congestive heart failure, CIRCULATION, 99(16), 1999, pp. 2113-2117
Citations number
36
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-Impaired endothelium-dependent, nitric oxide (NO)-mediated vasod
ilation may contribute to increased vasomotor tone in patients with heart f
ailure. Whether decreased endothelium-dependent, NO-mediated vasodilation i
n patients with heart failure is due to decreased synthesis or increased de
gradation of NO is unknown.
Methods and Results-To specifically assess the synthetic activity of the L-
arginine-NO metabolic pathway, urinary excretion of [N-15]nitrates and [N-1
5]urea was determined after a primed continuous intravenous infusion of L-[
N-15]arginine (40 mu mol/kg) in 16 patients with congestive heart failure a
nd 9 age-matched normal control subjects at rest and during submaximal trea
dmill exercise. After infusion of L-[N-15]arginine, 24-hour urinary excreti
on of N-15]nitrates was decreased in patients with congestive heart failure
at rest (2.2+/-0.5 versus 8.0+/-2.3 mu mol/24 h) and during submaximal exe
rcise (2.4+/-1.2 versus 11.4+/-4.0 mu mol/24 h) compared with control subje
cts (both P<0.01). After infusion of L-[N-15]arginine, 24-hour urinary excr
etions of [N-15]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 vasodilati
on in patients with congestive heart failure.