PROSTACYCLIN GENERATION BY CULTURED HUMAN VASCULAR ENDOTHELIAL CELLS WITH REFERENCE TO ANGIOTENSIN I-CONVERTING ENZYME

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Prostacyclin (PGI_2) generation has been known to be regulated by several endogenous vasoactive substances, and in this study the relationship between angiotensin I-converting enzyme (ACE) related substances and PGI_2 generation was investigated using cultured human vascular endothelial cells. Addition of angiotensin I(AI) or bradykinin(BK) enhanced PGI_2 generation and increased the level of ACE activity in the culture medium, while the addition of ACE inhibitor (captopril) caused a dose dependent suppression of PGI_2 generation and ACE activity. The enhancement of PGI_2 generation induced by AI or BK was not affected by pretreatment with captopril, and angiotensin II(AII) did not show any effect on either PGI_2 generation or ACE activity. Through these experimental results, the conversion of AI to AII by ACE was considered not to cause the enhancement of PGI_2 generation. Captopril solely inhibited PGI_2 generation and the reported hypothesis that captopril enhances PGI_2 generation by the accumulation of AI or BK via inhibition of ACE was not confirmed in this experimental system. Rather, it is proposed that AI or BK induced PGI_2 generation may be regulated by the increased breakdown of AI or BK, as an autoregulation mechanism, that is derived from increased ACE activity by AI or BK.
社団法人日本循環器学会の論文
1986-03-20