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Several observational studies suggest that greasy fish may reduce cardiovascular risk, whose benefits have been attributed to the presence Omega-3 polyunsaturated fatty acids (OM3FA). However, there are some randomized controlled trials (RCTs) that have shown contradictory results concerning the cardiovascular benefits of OM3FA. Analyzing these RCTs we found that the use of olive oil in some RCTs could be responsible for contradictory results, since both. since both olive oil and OM3FA, in addition to reduce triglycerides, have anti-platelet and anti-inflammatory activities, considered important for the stabilization of atherosclerotic plaques. This pharmacodynamic profile may have a cardio protective effect that was confirmed by several RCTs. Therefore, olive oil seems an active substance, and its use might have reduced the differences between groups masking the efficacy of OM3FA. This inferred lack of OM3FA cardiovascular benefits due to bias induced by a "false placebo" control, raises epistemological considerations on the choice of placebos that always should be pharmacologically inert substances. More studies are necessary to clarify the real efficacy of OM3FA that is more innocuous than many medicines, but it seems useful in future RCTs the use of a truly inert substance as a placebo, as well as the outline of a semi quantitative dose-response curve suggestive of a causal nexus between active substances and their outcomes., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Several compounds including lipopolysaccharide and sympathomimetics stimulate the expression of the inducible nitric oxide synthase in vascular smooth muscle cells. We evaluated the effect of clenbuterol on nitric oxide (NO) production by vascular smooth muscle cells of the rat aorta in culture. Wistar rats were divided into three diet groups (control, clenbuterol and washout). Aortic vascular smooth muscle cells from rats from these 3 diet groups were cultured in the presence and absence of lipopolysaccharide and/or beta-adrenoceptor agonists. NO release was measured by Griess reagent. Clenbuterol or salbutamol added to cells from control rats potentiated lipopolysaccharide-induced NO release. Cells from rats fed on clenbuterol, in a medium without beta-adrenoceptor agonists, showed a similar potentiation, even after a 10-day washout period. The addition of beta-adrenoceptor agonists to the latter cells did not increase NO production. NG-Nitro-L-arginine decreased nitrite production in lipopolysaccharide-stimulated cells. Our results demonstrate that dietary clenbuterol has a persistent 'ex vivo' effect on lipopolysaccharide-induced NO production by cultured vascular smooth muscle cells.