Blumberg A L, Nishikawa K, Denny S E, Marshall G R, Needleman P
Circ Res. 1977 Aug;41(2):154-8. doi: 10.1161/01.res.41.2.154.
We examined the ability of the angiotensins (A I, A II, A III) to release a prostaglandin E (PGE)-like substance in the isolated Krebs' perfused kidney and mesenteric vasculature of the rabbit by parallel bioassay. In the kidney, the order of potency for PGE release was A II greater than A III greater than A I with ED50's of 36, 100, and 500 pmol, respectively. In the mesenteric preparation, on the other hand, the order of potency was A III greater than A II greater than A I with ED50's of 75, 125, and 500 pmol, respectively. During one transit through the kidney 72-76% of bioassayable A I and A II was degraded. A III was 89% metabolized. In contrast, the mesenteric vasculature inactivated only 27% of A II and 23% of A III. This data suggests an inverse relationship between renal peptide degradation and PGE release. For characterization of the renal angiotensin receptor-mediating PGE release, dissociation constants (KB) of the competitive angiotensin antagonists [IIe7]-A III and [Sar1, IIe3]-A II were determined with each angiotensin. KB values of the individual antaganists were not significantly different with A I, A II, or A III; this finding suggests that one renal angiotensin receptor is involved with PGE release.
我们通过平行生物测定法，研究了血管紧张素（AI、AII、AIII）在兔离体Krebs灌注肾和肠系膜血管系统中释放前列腺素E（PGE）样物质的能力。在肾脏中，PGE释放的效力顺序为AII大于AIII大于AI，其半数有效剂量（ED50）分别为36、100和500皮摩尔。另一方面，在肠系膜制剂中，效力顺序为AIII大于AII大于AI，其ED50分别为75、125和500皮摩尔。在肾脏中循环一次，72 - 76%的可生物测定的AI和AII被降解。AIII有89%被代谢。相比之下，肠系膜血管系统仅使27%的AII和23%的AIII失活。这些数据表明肾脏肽降解与PGE释放之间存在反比关系。为了表征介导PGE释放的肾血管紧张素受体，用每种血管紧张素测定了竞争性血管紧张素拮抗剂[IIe7]-AIII和[Sar1,IIe3]-AII的解离常数（KB）。单个拮抗剂的KB值与AI、AII或AIII相比无显著差异；这一发现表明一种肾血管紧张素受体参与了PGE的释放。
