動脈硬化
Online ISSN : 2185-8284
Print ISSN : 0386-2682
ISSN-L : 0386-2682
虚血性心臓病の成因に関する研究
β-遮断剤のリポ蛋白代謝に及ぼす影響
上田 正人南部 征喜水口 宣信万江 治夫仮屋 純人太田 勝利戸嶋 裕徳木村 登Teturo INOUE
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1975 年 3 巻 1 号 p. 31-36

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Our previous report had been demonstrated that spontaneously hypertensive rat (SHR), in comparisson with normotensive Wistar rat, had the plasma lipoprotein characterized by a higher value of triglyceride (TG) in very low density lipoprotein (VLDL)/TG in low density lipoprotein (LDL) ratio. It is likely that β-adrenergic mechanism have an influence on the plasma lipoprotein in SHR. This study was designed to determine the effects of propranolol and pindolol on the plasma lipoprotein metabolism using double isotope method in SHR.
Radioactivities of total plasma lipids at three hours after infusion of 14C-1-Palmitate were lower in both beta-blockade groups than in untreated group. This result was suggested that utilization of free fatty acid (FFA) into lipidsynthesis system was diminished by beta-blockade. Additionally, pindolol treated group compared with both propranolol treated group and untreated group was showed a decrease in the specific activity of VLDL-TG at one hour with a relative increase in that of LDL-TG at three hours.
On the other hand, specific activity of lipoprotein-protein from infusion of 3H-2-Glycine were increased in LDL for pindolol treated group. But this finding was not observed in other groups. Therefore, it was suggested that pindolol accelerated the catabolism of VLDL to LDL through hydrolysis of TG. Moreover, pindolol treated group showed a higher incorporation of 14C-1-Palmitate into phospholipid (PL) in high density Lipoproteins (HDL2-PL) than into HDL3-PL at one hour which it was coincided with the changes of VLDL-TG. It might be possible that pindolol modulates the removal of HDL2-PL which plays a role in VLDL-TG hydrolyzed with lipoprotein lipase. These mechanism appears to be mediated by a β-adrenergic receptor.

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© 一般社団法人 日本動脈硬化学会
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