AORTIC PHOSPHOLIPID DEACYLATION-REACYLATION CYCLE IN SPONTANEOUSLY HYPERTENSIVE RATS

In vitro synthesis of prostaglandins (PG[prostaglandin]I2, PGE2, and PGF2.alpha.), phospholipase A2 activity and incorporation of arachidonate into phospholipids and neutral lipids was studied in the aortas of 20-24 wk old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar-Kyoto rats (WKY). PGI2 was by far the predominant species synthesized by aortic rings and homogenates in both animal groups. SHR and higher activities for all PG in either rings or homogenates of aortas. Because substrate availability is a key step in PG-synthesis, phospholipase A2 activity was studied in aortic homogenates using [2-14C]arachidonyl phosphatidylcholine as substrate. Enhanced activity was found in SHR (74 .+-. 8 vs. 34 .+-. 4 pmol-mg-1-2 h-1 in WKY, P < 0.01). Esterification of [14C]arachidonate into tissue phospolipids was increased in SHR (560 .+-. 107 vs. 327 .+-. 43 pmol-2 mg-1-h-1 in WKY, P < 0.01). Esterification of this fatty acid into neutral lipids was similar in the 2 experimental groups. More than 90% of the labeled tissue phospholipid was phosphatidylcholine, and the esterification occurred in the position 2 of the lecithin molecule. Addition of exogenous lysophosphatidylcholine as an acceptor of [14C]arachidonyl-CoA showed that reacylation of lysophosphatides is not induced in the SHR. In SHR, increased PG synthetase activity apparently is associated with enhancement of phospholipase A2. The higher arachidonate incorporation into phospholipids may be achieved by pathways other than reacylation of lysophosphatides.