Dietary linoleic acid deprivation: effects on blood pressure and PGI2 synthesis

Abstract

The possible role of arachidonic acid metabolites in the regulation of arterial blood pressure was investigated in rats receiving 0, 5, or 9 energy (en) % linoleic acid in their diet (groups 1-3) over 6 wk. In group 1 animals, systolic arterial blood pressure significantly increased from 100.5 +/- 2.0 to 110.6 +/- 3.1 mmHg (P less than 0.01) after 6 wk of dietary linoleic acid deprivation, whereas no effect on blood pressure was observed in group 2 and 3 animals receiving dietary linoleic acid supplements. Generation of prostacyclin (PGI2)-like activity by isolated aorta from rats fed the different diets was determined using a platelet-aggregation bioassay following incubation of aortic tissue for 12, 15, and 30 min, respectively. In isolated aorta from rats fed the 5 en% linoleic acid, production of PGI2 was 55.9 +/- 1.2, 70.5 +/- 2.6, and 90.9 +/- 3.6 pmol/mg over the three incubation periods. In group 1 animals, a significant suppression of PGI2 generation to 35.4 +/- 1.5, 41.1 +/- 1.7, and 55.0 +/- 1.2 pmol/mg (P less than 0.005) was observed, whereas PGI2 production was unaltered in aortic tissue from group 3 animals. In contrast, plasma concentrations of circulating thromboxane B2 were highest in group 1 animals (2.15 +/- 0.38 pmol/ml) and measured 1.28 +/- 0.17 and 0.83 +/- 0.10 pmol/ml in group 2 and 3 animals, respectively. Our results demonstrate that dietary deprivation of the arachidonic acid precursor linoleic acid increases arterial blood pressure that is associated with a suppression of vascular PGI2 synthesis and, most likely, a secondary rise in circulating thromboxane concentrations.

Influence of Dietary Fats Upon Systolic Blood Pressure in the Rat

“…In the rat, dietary LA deprivation increases blood pressure (Rosenthal et al, 1974;ten Hoor & van de Graaf, 1978;Schoene et al, 1980), whilst supplementation has a hypotensive effect (ten Hoor & van de Graaf, 1978;Schoene et al, 1980;Smith-Barbaro et al, 1980;MacDonald et al, 1981). The difference in blood pressure between animals on a low LA diet (coconut oil) and a high LA diet (corn oil), in the present study, was 52 mm Hg This difference was of a greater magnitude than previously reported in studies comparing rats on a normal LA diet and an LA deficient diet (MacDonald et al, 1981;Dusing et al, 1983).…”

“…LA deprivation in the rat is associated with lower urinary excretion of prostacyclin metabolites (ten Hoor & van de Graaf, 1978), concomitant with raised blood pressure. Circulating levels of TXA, are lowered in LA deficient rats on increasing arterial pressure (Dusing et al, 1983). LA supplementation increases prostaglandin production from the perfused rat aorta (ten Hoor & van de Graaf, 1978), whilst generation of renal prostaglandins by isolated rat glomeruli is LA-dependent (Dusing et al, 1990).…”

“…High fat diets, regardless of the type of fat used, increase blood pressure (Bursztyn et al, 1972;Bursztyn & Firth, 1975). n-6 (MacDonald et Dusing et al, 1983) and n-3 (Scherhag et al, 1982) fatty acid classes both appear to have specific modulatory effects.…”

Prostacyclin and Hypertension

“…Blood Pressure Increase Induced by Linoleic Acid Deficiency An increased blood pressure can also be induced in normotensive Sprague-Dawley rats by withdrawing linoleic acid from the diet [52]. In these studies a continuous and statistically significant increase in systolic blood pressure Systolic blood pressure (mmHg) Fig.…”

Salt Loading Increases Urinary Excretion of Linoleic Acid Diols and Triols in Healthy Human Subjects

“…8 -10 LA is a precursor of arachidonic acid, and it has been proposed that the effects of LA on blood pressure and salt excretion may be mediated through the production of various cytochrome P450 (CYP) eicosanoids and/or prostaglandins, including the epoxyeicosatrienoic acids (EETs) [11][12][13][14] and the prostacyclin metabolite 6-keto-prostaglandin (PG) F1␣. 15,16 Inhibition of CYP-mediated EET production has been associated with the development of hypertension in rats. 11 Dietary salt loading upregulates CYP2C23 in rats, increasing EET production and inhibiting Na ϩ reabsorption, whereas low-salt diets suppress this enzyme.…”