Diet affects significantly the incidence and severity of cardiovascular diseases and fatty acid intake, in its qualitative as well as quantitative aspects, and influences several risk factors including cholesterol (total, LDL and HDL), triglycerides, platelet aggregation and blood pressure, as evidenced in the 2001 WHO report. This review focuses on the qualitative concern of lipid intake, the various classes of fatty acids of the lipid fraction of the diet, saturated, monounsaturated and polyunsaturated, and their effects on blood pressure. Saturated fat have a bad file and several experimental studies in the rat showed a progressive increase in blood pressure in response to a highly saturated diet. Moreover, a highly saturated diet during gestation led to offspring which, when adults, presented a gender-related hypertension. The mechanism of this effect may be related to the polyunsaturated/saturated ratio (p/s). During the past 20 years, trans fatty acids have been suspected of deleterious health effects, but the investigations have shown that these fatty acids display a biological behaviour close to that of saturated fatty acids (SFA). Moreover, epidemiological investigations did not confirm the relationship between trans fatty acids and cardiovascular pathology. Polyunsaturated fatty acids have been shown to exert a positive action on hypertension. This effect could be attributed to the alteration of the p/s, but mainly to the omega3 polyunsaturated fatty acids (PUFAs). The comparison of several animal models led to the conclusion that long-chain omega3 PUFAs (eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)) can prevent the increase in blood pressure and reduce established hypertension, but the efficient dose remains an object of discussion. Moreover, the two long-chain omega3 PUFAs, EPA and DHA, display specific effects, which vary with the aetiology of hypertension, because their mechanism of action is different. DHA acts on both blood pressure and heart function (heart rate and ECG) and interferes with the adrenergic function. Conversely, EPA, which is not incorporated in cardiac phospholipids, has no effect on the heart and its mechanism of action is largely unknown. Although it is accepted by the scientific community that the intake of EPA and DHA needs to be increased, we will have to discover new ways to do it, since marine products are the main source of these fatty acids, and this source is not inexhaustible.