Effect of omega-3 fatty acids on the vascular response to angiotensin in normotensive men

There is a widespread interest in fish oil as a dietary supplement and possible nonpharmacologic adjunct in the treatment of hypertension. The effect of dietary fish oil on blood pressure is controversial and the effect on systemic hemodynamics and regional vascular reactivity in humans is unknown....

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Published inThe American journal of cardiology Vol. 70; no. 15; pp. 1347 - 1352
Main Authors Kenny, Dermot, Warltier, David C., Pleuss, Joan A., Hoffmann, Raymond G., Goodfriend, Theodore L., Egan, Brent M.
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 15.11.1992
Elsevier
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Summary:There is a widespread interest in fish oil as a dietary supplement and possible nonpharmacologic adjunct in the treatment of hypertension. The effect of dietary fish oil on blood pressure is controversial and the effect on systemic hemodynamics and regional vascular reactivity in humans is unknown. To address these questions, a doubleblind, placebo-controlled, crossover study on the effect of dietary fish oil substitution was performed during a carefully controlled diet in 8 normotensive men. Systemic hemodynamics and the forearm vascular response to intrabrachial artery infusions of norepinephrine, phentolamine and angiotensin II were obtained. Compared with a safflower oil placebo, dietary fish oil had no effect on cardiac output (6.42 ± 0.38 vs 6.87 ± 0.28 liters/ min, p = not significant) or 24-hour blood pressure (122/68 ± 3/3 vs 122/68 ± 3/2 mm Hg, p = not significant). The vascular response to norepinephrine and phentolamine was unchanged. Fish oil, however, significantly (p < 0.05) reduced forearm vascular resistance responses to angiotensin II. These changes were associated with a reduction in plasma triglycerides (64 ± 9 vs 39 ± 4 mg/dl, p = 0.02) and an increase in plasma eicosapentaenoic acid levels (0.51 ± 0.25 vs 1.72 ± 0.35 μM, p < 0.05). Substitution of a moderate dose of fish oil for fat in a “Western diet” selectively attenuates the vascular response to angiotensin independently of changes in α-adrenergic vasoconstriction or systemic hemodynamics.
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ISSN:0002-9149
1879-1913
DOI:10.1016/0002-9149(92)90773-R