The role of nitric oxide in the electrical and mechanical activities of the
rat portal vein was examined in circular muscle preparations with intact e
ndothelium that were isolated from the longitudinal muscle layer. In contra
st to the longitudinal muscle preparation, the circular muscle preparation
did not show spontaneous phasic contraction. Inhibition of nitric oxide syn
thesis by N-omega-nitro-L-arginine (L-NNA) induced a tonic contraction. The
contraction was inhibited by L-arginine, sodium nitroprusside or nifedipin
e. L-NNA did not induce contraction in endothelium-damaged preparations. Th
e membrane potential of smooth muscle cells recorded in endothelium-intact
preparations showed sporadic action potentials. L-NNA increased the frequen
cy of action potentials without changing the resting membrane potential. Th
e action potentials were inhibited by nifedipine. In the presence of L-NNA,
sodium nitroprusside decreased the frequency of the action potentials with
out changing the resting membrane potential. These results indicated that c
ontraction of rat portal vein circular muscles is inhibited tonically by ni
tric oxide, at least partly through inhibition of electrical activity.