Further studies on the mechanism of increased blood pressure during dietary linoleic acid deprivation.
The present studies investigate the changes in blood pressure and excretory renal function in rats during dietary linoleic acid deprivation. Four groups of animals were fed isocaloric diets containing 10 en % saturated fat and either 5 en % linoleic acid (groups I and III) or 5 en % oleic acid (groups II and IV). In addition, groups I and II received a chronic high intake of Na (greater than 5 mmol/day) while groups III and IV were Na restricted with an average Na intake of 0.7 mumol/day. Blood pressure significantly increased in the high salt, linoleic acid deprived group II and was unchanged in all three other groups of animals. De novo synthesis of prostaglandin E2 in rat kidney inner medullary homogenates in the four groups of animals at the end of the dietary protocol showed a marked dependency on Na balance with significantly (p less than 0.01) higher values in the Na restricted animals as well as on linoleic acid intake with significantly (p less than 0.01) higher values in the linoleic acid substituted animals. Urinary excretion of NaCl during acute expansion of the extracellular fluid volume with hypotonic saline was significantly impaired in the animals receiving oleic acid instead of linoleic acid. In a metabolic study, linoleic acid deprived animals retained Na from the first day of linoleic acid deprivation and blood pressure started to rise only after a substantial amount of Na had been retained. Our results show that linoleic acid deprivation suppresses renal arachidonic acid cyclooxygenase metabolism and impairs the renal ability to excrete an acute salt load. Impaired renal excretory function precedes the increase in blood pressure. Thus suppressed renal cyclo-oxygenase metabolism which impairs renal excretory function may be a crucial mechanism in the rise of blood pressure during dietary linoleic acid deprivation.
D000818:Animals; D002712:Chlorides / Q000652:urine; D004041:Dietary Fats / Q000378:metabolism*; D015232:Dinoprostone; D005260:Female; D006973:Hypertension / Q000209:etiology* / Q000378:metabolism; D007668:Kidney / Q000201:enzymology; D007679:Kidney Medulla / Q000378:metabolism; D008041:Linoleic Acids / Q000172:deficiency*; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D011458:Prostaglandins E / Q000096:biosynthesis; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000652:urine; D012965:Sodium Chloride / Q000378:metabolism
D002712:Chlorides; D004041:Dietary Fats; D008041:Linoleic Acids; D011458:Prostaglandins E; D012965:Sodium Chloride; D012964:Sodium; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone