Dietary Suppression of Prostaglandin Synthesis Does Not Accelerate Doca/Salt Hypertension in Rats

Codde, Jim; Croft, Kevin D.; Beilin, Lawrence J.

doi:10.1111/j.1440-1681.1987.tb01507.x

Cited by 10 publications

(3 citation statements)

References 38 publications

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“…Earlier studies have demonstrated both hypotensive and hypertensive effects of fish oils in humans and animals (Schoene et al, 1981;Scherhag et al, 1982;Ziemlanski et al, 1985;Codde et al, 1987;Bonaa et al, 1990). In contrast, the present study demonstrated no significant effect.…”

Section: Discussionmentioning

confidence: 93%

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Influence of Dietary Fats Upon Systolic Blood Pressure in the Rat

Langley‐Evans

Clamp

Grimble

et al. 1996

International Journal of Food Sciences and Nutrition

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Studies were performed to determine whether feeding diets with differing fatty acid content and composition had an influence on systolic blood pressure in the rat. Weanling male rats were fed standard laboratory chow (2.9% fat in total), or synthetic diets (10% fat in total) containing fish oil, butter, coconut oil or corn oil, for 5 weeks. Coconut oil and butter diets were rich in saturated fatty acids, whilst fish oil and corn oil were rich in the n-3 and n-6 unsaturated fatty acids respectively. Systolic blood pressure was measured using an indirect tail-cuff method at the end of the feeding period, and compared to a group of weanling rats. Feeding the different diets did not alter the growth of the rats, so all animals were of similar weights at the time of blood pressure determination. Control (chow fed) animals, at nine weeks of age, had higher systolic blood pressures than the weanling, baseline control group. Fish oil fed rats had similar pressures to the chow fed rats. Corn oil fed rats had significantly lower systolic pressures than the controls. The rats led the diets rich in saturated fatty acids (butter and coconut oil) had significantly higher blood pressures than all other groups. Systolic blood pressure was found to be significantly related to the dietary intakes of saturated and unsaturated fatty acids. The dietary intake of linoleic acid was significantly higher in corn oil fed rats than in other groups. Systolic blood pressure was inversely related to linoleic acid intake. Feeding a diet rich in saturated fatty acids significantly increases blood pressure in the rat. A high intake of n-6 fatty acids, and in particular linoleic acid, appears to have a hypotensive effect. Prenatal exposure of the rats to a maternal low protein diet, abolished the hypertensive effects of the coconut oil diet and the hypotensive effect of the corn oil diet upon young adult females. The intrauterine environment may, therefore, be an important determinant of the effects of these fatty acids on blood pressure in later life.

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Section: Discussionmentioning

confidence: 93%

“…Reductions of blood pressure in this strain, induced by n-3 fatty acids, are accompanied by a suppression of prostaglandin (PGE,, PGF2) production (Schoene et al, 1981). When SHR rats are salt loaded however, their ability to excrete the salt is inhibited by EPA and DHA, leading to a rise in blood pressure (Codde et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

Influence of Dietary Fats Upon Systolic Blood Pressure in the Rat

Langley‐Evans

Clamp

Grimble

et al. 1996

International Journal of Food Sciences and Nutrition

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“…In this model, the chronic subcutaneous infusion of aldosterone to adult male Sprague-Dawley rats maintained on a normal or a high sodium diet was shown to cause a mild and gradual increase in systohc arterial pressure over a period of 4 weeks. The chronic administration of aldosterone was also associated with a rise in the urinary levels of PGE2, 6-oxo-PGFi a , and TXB2, an observation that suggests aldosterone stimulates the biosynthesis of PGE2 and PGI 2 the biosynthesis of prostanoids in various models of mineralocorticoid-induced hypertension. 1 -319 On the other hand, aldosterone did not seem to exert any significant effects on the systemic production of PGIâ s judged by its lack of influence on the urinary excretion of 2,3-dinor-6-oxo-PGFi <r The mechanism by which aldosterone stimulates the biosynthesis of prostanoids in the kidney in vivo is unclear but may be related to its known effects on the activity of phospholipase A 2 and the deacylation/reacylation of phospholipids in vitro.…”

Section: Discussionmentioning

confidence: 94%

Prostanoids and aldosterone-induced mild experimental hypertension in rats.

et al. 1990

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The goal of this study was to determine the role of prostanoids in a new model of mineralocorticoid-dependent hypertension induced by the subcutaneous infusion of aldosterone (1 fig/hT) to normal male Sprague-Dawley rats. This regimen caused a mild and gradual increase in systolic pressure over a period of 4 weeks (113±1 vs. 137±3 mm Hg) and was associated with an increase in the in vivo formation of prostaglandins I 2 and Ej and of thromboxane A 2 in the kidney. High sodium intake induced a fall in the urinary levels of prostaglandin E? aQ d a rise in the arterial pressure of control rats (126±1 vs. 113±1 mm Hg) but did not influence aldosterone-induced hypertension. Indomethacin (3.0 nig/kg/day) caused a profound inhibition of the in vivo synthesis of prostaglandin I 2 and thromboxane A 2 without modifying the renal production of prostaglandin E 2 . Although indomethacin exerted no effect on aldosterone-induced hypertension in rats fed a normal diet, it caused a further rise in systolic pressure in aldosterone-treated rats fed a high sodium diet (157±6 vs. 140±4 mm Hg). The results of this study in a model of aldosterone-induced mild hypertension in the rat indicate that 1) aldosterone exerts a stimulatory effect on the renal synthesis of prostanoids, particularly prostaglandin E?; 2) thromboxane A 2 and prostaglandin I 2 do not seem to play a role in aldosterone-induced hypertension under conditions of normal dietary salt intake, whereas the role of prostaglandin E 2 is unclear; 3) there is enough sodium in a normal diet to allow for the maximal expression of the hypertensive effect of aldosterone; 4) prostaglandin I 2 seems to play a significant role in modulating the cardiovascular impact of a high sodium diet in aldosteronetreated rats; and 5) the renal biosynthesis of prostaglandin E 2 is particularly resistant to the inhibitory effect of indomethacin in vivo. induced a further fall in blood pressure, suggesting that the concomitant formation of a pressor prostanoid could contribute to mineralocorticoid-induced severe hypertension. However, these models, which combine mineralocorticoid administration with uninephrectomy or the addition of sodium chloride to drinking water at an isosmolar or hyperosmolar concentration, are situations rarely encountered in clinical medicine.The objective of the present study was to investigate the role of prostanoids in a model of mineralocorticoidinduced hypertension that resembles more closely human primary aldosteronism. The results include the influence of aldosterone, dietary salt, and indomethacin on the systolic arterial pressure and the in vivo biosynthesis of PGI 2 and PGE2 and of TXA 2 , in a model of hypertension induced by the chronic subcutaneous administration of aldosterone in normal Sprague-Dawley rats.

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Cardiovascular activity1

Vogel

Schölkens

et al. 2002

Drug Discovery and Evaluation

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Dietary Suppression of Prostaglandin Synthesis Does Not Accelerate Doca/Salt Hypertension in Rats

Cited by 10 publications

References 38 publications

Influence of Dietary Fats Upon Systolic Blood Pressure in the Rat

Influence of Dietary Fats Upon Systolic Blood Pressure in the Rat

Prostanoids and aldosterone-induced mild experimental hypertension in rats.

Cardiovascular activity1

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