Bretherton K N, Day A J, Skinner S L
Atherosclerosis. 1976 Sep;24(3):431-40. doi: 10.1016/0021-9150(76)90135-0.
The effect of prior hypertension on lipid synthesis in the thoracic aortae of normal-fed and cholesterol-fed rabbits was studied in vitro using[1(-14)C] acetate and [32P] phosphate as lipid precursors. In normally fed rabbits, prior hypertension did not increase the incorporation of the labelled precursors into either phospholipid or neutral lipid. In cholesterol-fed rabbits, hypertension increased the incorporation of [32P] phosphate into phosphatidyl-choline and of [1(-14)C-acetate into cholesterol ester. The increased incorporation of [1(-14)C] acetate into cholesterol ester was accompanied by an increase in intimal total cholesterol concentration. For both normotensive and hypertensive cholesterol-fed rabbits there was a close correlation between cholesterol esterification and total cholesterol concentration of the thoracic intima. It is concluded that the increase in aortic lipid synthesis in hypertensive cholesterol-fed rabbits is secondary to the increased cholesterol accumulation induced by hypertension rather than to a direct stimulation of arterial wall lipid synthesis by hypertension per se.
采用[1(-14)C]乙酸盐和[32P]磷酸盐作为脂质前体，在体外研究了既往高血压对正常喂养和高胆固醇喂养兔子胸主动脉脂质合成的影响。在正常喂养的兔子中，既往高血压并未增加标记前体掺入磷脂或中性脂质的量。在高胆固醇喂养的兔子中，高血压增加了[32P]磷酸盐掺入磷脂酰胆碱以及[1(-14)C]乙酸盐掺入胆固醇酯的量。[1(-14)C]乙酸盐掺入胆固醇酯增加的同时，内膜总胆固醇浓度也增加。对于血压正常和高血压的高胆固醇喂养兔子，胆固醇酯化与胸内膜总胆固醇浓度之间均存在密切相关性。得出的结论是，高血压高胆固醇喂养兔子主动脉脂质合成增加是高血压所致胆固醇蓄积增加的继发结果，而非高血压本身直接刺激动脉壁脂质合成所致。
