Okamoto H
Department of Cardiovascular Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1988 Sep;63(5):796-804.
The purpose of this study is to examine the relationship between lipid alterations in renal membrane of SHRSP and the progress of hypertension. Phospholipase A2 activity, prostaglandin E2 synthesis, phospholipids and phospholipid fatty acids were investigated in renal cortex and medulla of male SHRSP at the ages of 5, 10, 20 and 40 weeks, and compared with age-matched Wistar-Kyoto rats (WKY). In renal membrane of SHRSP, phospholipase A2 activity enhanced and PGE2 synthesis increased both in the renal cortex and the medulla after 20 weeks of age. Phospholipids, especially phosphatidylcholine and phosphatidylethanolamine, and arachidonate were decreased in cortex after 20 weeks and in medulla after 10 weeks. Moreover, to determine the effect of pressure load on lipid alterations, SHRSP that received an antihypertensive treatment with hydralazine or nicardipine or enalapril for 5 weeks were compared with those without treatment. Antihypertensive treatment prevented the blood pressure from rising and suppressed decreases of phospholipids and arachidonate in phospholipid. In conclusion, these results might suggest that enhanced phospholipase A2 cause by hypertension activate the arachidonic acid cascade and increase prostaglandin synthesis, which might have an homeostatic action to lower the blood pressure in SHRSP. On the other hand, decreases of phospholipids and arachidonate may provide an explanation for the membraneous structural abnormalities in SHRSP. Antihypertensive treatments prevent these alterations, though they have different actions in SHRSP.