Düsing R, Scherf H, Landsberg G, Glänzer K, Kramer H J
Ann Clin Res. 1984;16 Suppl 43:103-8.
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.
本研究调查了大鼠在饮食中缺乏亚油酸期间血压和肾脏排泄功能的变化。将四组动物喂食含10能量%饱和脂肪且分别含5能量%亚油酸（I组和III组）或5能量%油酸（II组和IV组）的等热量饮食。此外，I组和II组长期高钠摄入（大于5 mmol/天），而III组和IV组钠摄入受限，平均钠摄入量为0.7 μmol/天。高盐、缺乏亚油酸的II组血压显著升高，而其他三组动物血压未变。在饮食方案结束时，四组动物大鼠肾内髓匀浆中前列腺素E2的从头合成显示出对钠平衡的显著依赖性，钠摄入受限的动物中值显著更高（p<0.01），同时也依赖于亚油酸摄入，亚油酸替代的动物中值显著更高（p<0.01）。用低渗盐水急性扩充细胞外液容量期间，摄入油酸而非亚油酸的动物NaCl尿排泄显著受损。在一项代谢研究中，缺乏亚油酸的动物从缺乏亚油酸的第一天起就潴留钠，且仅在潴留大量钠后血压才开始升高。我们的结果表明，缺乏亚油酸会抑制肾脏花生四烯酸环氧化酶代谢，并损害肾脏排泄急性盐负荷的能力。肾脏排泄功能受损先于血压升高。因此，抑制肾脏环氧化酶代谢从而损害肾脏排泄功能可能是饮食中缺乏亚油酸期间血压升高的关键机制。
