I'm assuming you mean question #128. If not, please clarify.
So, normally, when intact endothelial cells are exposed to acetylcholine, they release Nitric Oxide (NO), which thus causes the blood vessels to relax, or dilate. However, if the production of NO was interrupted (by, say, an inhibitor of the enzyme that synthesizes it), then it would not be able to produce its vasodilating effects.
Well, this is exactly what the situation is describing. By introducing a saturating concentration of the inhibitor L-NMMA (in the text beneath the graphs L-NMMA is stated to be an inhibitor of NO synthase), NO is prevented from being synthesized. Thus, the vessels would not be able to relax as they normally would, and as a result the tension of the aortic ring would increase.