Background
Basal release of nitric oxide (
NO
) from the vascular endothelium regulates the tone of muscular arteries and resistance vasculature. Effects of
NO
on muscular arteries could be particularly important during exercise when shear stress may stimulate increased
NO
synthesis.
Methods and Results
We investigated acute effects of
NO
synthase inhibition on exercise hemodynamics using
N
G
‐monomethyl‐
l
‐arginine (
l
‐
NMMA
), a nonselective
NO
synthase ‐inhibitor. Healthy volunteers (n=10, 5 female, 19–33 years) participated in a 2‐phase randomized crossover study, receiving
l
‐
NMMA
(6 mg/kg, iv over 5 minutes) or placebo before bicycle exercise (25–150 W for 12 minutes). Blood pressure, cardiac output (measured by dilution of soluble and inert tracers) and femoral artery diameter were measured before, during, and after exercise. At rest,
l
‐
NMMA
reduced heart rate (by 16.2±4.3 bpm relative to placebo,
P
<0.01), increased peripheral vascular resistance (by 7.0±1.4 mmHg per L/min,
P
<0.001), mean arterial blood pressure (by 8.9±3.5 mmHg,
P
<0.05), and blunted an increase in femoral artery diameter that occurred immediately before exercise (change in diameter: 0.14±0.04 versus 0.32±0.06 mm after
l
‐
NMMA
and placebo,
P
<0.01). During/after exercise
l
‐
NMMA
had no significant effect on peripheral resistance, cardiac output, or on femoral artery diameter.
Conclusions
These results suggest that
NO
plays little role in modulating muscular artery function during exercise but that it may mediate changes in muscular artery tone immediately before exercise.
Inhibition of Nitric Oxide but Not Prostacyclin Prevents Poststenotic Dilatation in Rabbit Femoral Artery
