Jk. Barclay et Ne. Woodley, NITRIC-OXIDE SYNTHASE INHIBITORS DO NOT ALTER FUNCTIONAL HYPEREMIA INCANINE SKELETAL-MUSCLE, Canadian journal of physiology and pharmacology, 72(9), 1994, pp. 1035-1041
To test the hypothesis that endothelium-derived products contribute to
functional hyperemia in skeletal muscle, we infused nitric oxide synt
hase inhibitors, either 200 mu M N omega-nitro-L-arginine (NNA) (N = 4
) or 1 mM N gamma-monomethyl-L-arginine (NMMA) (N = 4), before and dur
ing 6 min of 4 Hz stimulation of canine gastrocnemius in situ. We infu
sed saline (N = 4) as a control. NNA significantly decreased steady-le
vel resting flow by 3.8 +/- 0.4 mL.kg(-1).s(-1). The increase in flow
from rest to 5 min of stimulation was not changed by the nitric oxide
synthase inhibitors. We also stimulated muscles for 60 min either with
saline infusion (N = 4) or with the infusion of saline during the fir
st 15 min and NNA for the remaining 45 min (N = 4). There was no diffe
rence in the flow during contractions. To clarify the effect of these
inhibitors on canine vessels, we challenged rings of canine femoral ar
tery with and without endothelium with acetylcholine and bradykinin (b
oth 1 mu M) before and after the addition of NNA and NMMA (both 10 mu
M). The nitric oxide synthase inhibitors decreased the relaxation acco
mpanying acetylcholine. Both inhibitors caused only endothelium-intact
rings to contract. Thus, the presence of a nitric oxide synthase inhi
bitor identified an endothelium-dependent contribution to the regulati
on of blood flow to skeletal muscle at rest but had no effect on funct
ional hyperemia.