Wan D C, Marley P D, Livett B G
Department of Biochemistry, University of Melbourne, Parkville, Victoria, Australia.
Neuropeptides. 1990 Jul;16(3):141-7. doi: 10.1016/0143-4179(90)90126-j.
The effects of angiotensin II on the expression of proenkephalin A (ProEnk A) mRNA and enkephalin release were examined in cultured bovine adrenal chromaffin cells. Exposure of chromaffin cells for 24h to 10 nM angiotensin II produced a more than 2-fold increase in cellular ProEnk A mRNA levels with a concomitant elevation in the levels of high molecular weight Met5-enkephalin-Arg6-Gly7-Leu8-like immunoreactivity in the culture medium. These stimulatory effects of angiotensin II on enkephalin release and mRNA expression were fully antagonized by the angiotensin II antagonist [Sar1, Ala8]-angiotensin II. The angiotensin II-induced increase in ProEnk A mRNA levels was also abolished by the RNA synthesis inhibitor actinomycin D. These results indicate that specific angiotensin II receptor activation is responsible for stimulating transcription of ProEnk A mRNA and enkephalin. Angiotensin II may therefore be involved in the long-term regulation of ProEnk A gene expression in the adrenal medulla.
在培养的牛肾上腺嗜铬细胞中，研究了血管紧张素II对前脑啡肽原A（ProEnk A）mRNA表达和脑啡肽释放的影响。将嗜铬细胞暴露于10 nM血管紧张素II 24小时，可使细胞内ProEnk A mRNA水平增加2倍以上，同时培养基中高分子量Met5-脑啡肽-Arg6-Gly7-Leu8样免疫反应性水平也随之升高。血管紧张素II拮抗剂[Sar1, Ala8]-血管紧张素II完全拮抗了血管紧张素II对脑啡肽释放和mRNA表达的这些刺激作用。RNA合成抑制剂放线菌素D也消除了血管紧张素II诱导的ProEnk A mRNA水平升高。这些结果表明，特定的血管紧张素II受体激活负责刺激ProEnk A mRNA和脑啡肽的转录。因此，血管紧张素II可能参与肾上腺髓质中ProEnk A基因表达的长期调节。
