The effect of dietary supplementation with linoleic and gammalinolenic acids on the pressor response to angiotensin II‐a possible role in pregnancy‐induced hypertension?

Abstract

Dietary supplementation with 3 g/day linoleic acid, 32 mg/day gammalinolenic acid and co‐factors for prostaglandin synthesis was given to 10 pregnant and 10 non‐pregnant subjects for a week. Their pressor response to the infusion of three doses of angiotensin II (AII) (pregnant: 4, 8, 16 ng kg‐1 min‐1: non‐pregnant: 1, 2, 4 ng kg‐1 min‐1) was then compared with that of 40 pregnant and 24 non‐pregnant controls who had not been given such supplementation. Dietary supplementation was not associated with changes in basal systolic or diastolic blood pressure or heart rate during the week of treatment in pregnant or non‐ pregnant subjects. Basal systolic blood pressure, diastolic blood pressure and heart rate values did not differ between the treated and untreated subjects in each group. The diastolic pressor response to AII was significantly less after treatment at all doses; the effect was more marked in the pregnant subjects. The systolic response to AII, normally less than the diastolic, was somewhat blunted in the treated pregnant patients at the two higher infusion doses. No significant effect was found in the non‐pregnant group. Evidence from other studies suggests that increasing plasma linoleic acid concentrations leads to increased plasma concentrations of epoprostenol (prostacyclin, PGI2) while increased availability of gammalinolenic acid is associated with a rise in prostaglandin E1 and E2 production. Pregnancy‐induced hypertension is associated with a diminished tissue production of both epoprostenol and E series prostaglandins, and with an enhanced pressor response to AII.(ABSTRACT TRUNCATED AT 250 WORDS)

Essential fatty acids and their metabolites could function as endogenous HMG-CoA reductase and ACE enzyme inhibitors, anti-arrhythmic, anti-hypertensive, anti-atherosclerotic, anti-inflammatory, cytoprotective, and cardioprotective molecules

“…Dietary supplementation with 3 gm/day of LA and 32 mg/day of GLA to pregnant and non-pregnant subjects showed that the diastolic pressor response to angiotensin-II was significantly less in the pregnant subjects compared to the non-pregnant subjects, suggesting that PUFAs modulate vascular tissue responses to angiotensin-II. This decreased response to angiotensin-II could be due to increased formation of PGE 1 and PGI 2 in fatty acid supplemented pregnant subjects [ 72 , 73 ]. In a model of hypertension induced by continuous infusion of angiotensin-II in the rat, subcutaneous administration of LA and EPA and DHA were found to be equally potent in reducing, by half, the rise in systolic blood pressure induced by angiotensin-II and these anti-hypertensive effects were not accompanied by any changes in the renal synthesis of PGI 2 or PGE 2 .…”

The effect of prostanoid precursors and inhibitors on platelet angiotensin II binding

“…TXA 3 appears less biologically active than TX A 2 and PGI 3 appears equipotent with PG I 2 . D ietary supplementation with evening primrose oil which contains linoleic and gamm alinolenic acid has already been shown to be associated with a diminution in the pressor response to infused AII (O' Brien et al, 1985). It is possible that manipulation of prostaglandins by the administration of prostanoid precursors (® sh oil and evening primrose oil) and a prostaglandin inhibitor (aspirin) may effect mem brane¯uidity and in turn accessibility of AII receptors.…”

“…Evening primrose oil was used in this pilot study as it has been previously demonstrated that its administration can be associated with a blunting of the pressor response to infused AII (O' Brien et al, 1985). However, neither evening prim rose oil taken on its own or in combination with aspirin signi® cantly reduced platelet AII binding.…”

Lipoxins, Resolvins, Protectins, Maresins, and Nitrolipids: Connecting Lipids, Inflammation, and Cardiovascular Disease Risk

“…Several studies suggested that PUFAs have modulatory influence on renin secretion and action, yet at times are independent of both renin secretion and PG formation [17,18]. Because the anti-hypertensive actions of PUFAs seem to be independent of formation of PGs, it is likely that fatty acids themselves are able to bring about this action.…”