Nakagawa M, Sawada S, Toyoda T, Takamatsu H, Tsuji H, Ijichi H
Clin Exp Hypertens A. 1987;9(2-3):405-8. doi: 10.3109/10641968709164206.
The regulation of prostacyclin (PGI2) generation by angiotensin I-converting enzyme (ACE) related substances was investigated using cultured human vascular endothelial cells. Angiotensin I (AI) or bradykinin (BK) increased PGI2 generation and ACE activity, while the ACE inhibitor, captopril decreased both of them, and angiotensin II (AII) did not show any effect. The increasing rate of PGI2 generation induced by AI or BK was not affected by the pretreatment with captopril. These results suggest that the accumulation of AI or BK via the inhibition of ACE by captopril did not cause the enhancement of PGI2 generation. Rather, it was proposed that the enhanced PGI2 generation by AI or BK might be regulated by ACE activation derived from these substances, as an autoregulation mechanism.
利用培养的人血管内皮细胞研究了血管紧张素I转换酶（ACE）相关物质对前列环素（PGI2）生成的调节作用。血管紧张素I（AI）或缓激肽（BK）可增加PGI2生成和ACE活性，而ACE抑制剂卡托普利则可降低二者，血管紧张素II（AII）则无任何作用。卡托普利预处理不影响AI或BK诱导的PGI2生成增加率。这些结果表明，卡托普利抑制ACE导致的AI或BK蓄积并未引起PGI2生成增强。相反，有人提出，AI或BK增强的PGI2生成可能受这些物质衍生的ACE激活调节，作为一种自动调节机制。
