Inhibition of nitric oxide synthesis by systemic N-G-monomethyl-L-arginineadministration in humans: Effects on interstitial adenosine, prostacyclin and potassium concentrations in resting and contracting skeletal muscle
U. Frandsen et al., Inhibition of nitric oxide synthesis by systemic N-G-monomethyl-L-arginineadministration in humans: Effects on interstitial adenosine, prostacyclin and potassium concentrations in resting and contracting skeletal muscle, J VASC RES, 37(4), 2000, pp. 297-302
Citations number
35
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
We examined whether the formation or the release of the vasodilators adenos
ine, prostacyclin (PGI(2)) and potassium (K+) increase in skeletal muscle i
nterstitium in response to nitric oxide synthase (NOS) inhibition. Five sub
jects performed one-legged knee extensor exercise at 30 W without (controls
) and with prior N-G-nitro-L-arginine methyl ester (L-NAME) infusion (4 mg/
kg, intravenously). Samples from the interstitial fluid were obtained at re
st, during exercise and after exercise with the microdialysis technique. In
terstitial adenosine in controls increased (p < 0.05) from 0.11 +/- 0.03 mu
mol/l at rest to 0.48 +/- 0.06 mu mol/l during exercise. Interstitial aden
osine during exercise in L-NAME was similar (p > 0.05) to controls. The 6-k
eto-prostaglandin F1 alpha concentration in controls was 1.17 +/- 0.20 ng/m
l at rest and increased (p < 0.05) to 1.97 +/- 0.30 ng/ml during exercise a
nd was further elevated (p < 0.05) to 2.76 +/- 0.38 ng/ml after exercise an
d these concentrations were not different (p > 0.05) in L-NAME. The interst
itial K+ concentration in controls increased (p < 0.05) from 4.1 +/- 0.1 mm
ol/l at rest to 9.5 +/- 0.5 mmol/l during exercise. The interstitial K+ con
centration during exercise (6.7 +/- 0.4 mmol/l) was lower (p < 0.05) in L-N
AME than in controls. The present findings demonstrate that the muscle inte
rstitial concentrations of adenosine, PGI(2) and K+ during exercise are not
increased with systemic NOS inhibition. Thus, the lack of effect of NOS in
hibition on the rate of blood flow to contracting human skeletal muscle doe
s not appear to be due to compensatory formation or release of adenosine, P
GI(2) and K+ in the muscle interstitium. The present study also supports a
role for PGI(2) in the regulation of blood flow during exercise. Copyright
(C) 2000 S.Karger AG, Basel.