Cordeiro R S, Assreuy J, Cunha F Q, Flores C A, Martins A M, Vasconcelos H N, Rothschild A M
Braz J Med Biol Res. 1982 Dec;15(6):405-11.
Plasma kininogen levels were significantly reduced in normal human blood, but not in cell-free human plasma, following 10 min in vitro exposure to, in order of decreasing effectiveness, 6 microM adrenaline, noradrenaline or isopropyl-noradrenaline. Phenoxybenzamine (0.1 mM), an alpha-receptor blocking drug, and 0.5 mM aspirin, an inhibitor of prostaglandin (PG) synthesis, inhibited the action of adrenaline, whereas 0.1 mM propranolol, a beta-receptor blocker, and 0.5 mM indomethacin, another inhibitor of the formation of PG, failed to do so. The results suggest that catecholamines are able to activate cell-mediated activation of the kallikrein system in human blood and that this process can be inhibited by aspirin.
在体外将正常人血液分别暴露于6微摩尔肾上腺素、去甲肾上腺素或异丙基去甲肾上腺素10分钟后（按效力递减顺序），血浆激肽原水平在正常人血液中显著降低，但在无细胞人血浆中未降低。α受体阻断药苯氧苄胺（0.1毫摩尔）和前列腺素（PG）合成抑制剂阿司匹林（0.5毫摩尔）可抑制肾上腺素的作用，而β受体阻断剂普萘洛尔（0.1毫摩尔）和另一种PG形成抑制剂吲哚美辛（0.5毫摩尔）则无此作用。结果表明，儿茶酚胺能够激活人血液中细胞介导的激肽释放酶系统的激活，且该过程可被阿司匹林抑制。
