Cornish K G, Joyner W L, Gilmore J P
Circ Res. 1979 Apr;44(4):540-4. doi: 10.1161/01.res.44.4.540.
Kininase II (angiotensin I-converting enzyme) is generally accepted to be the enzyme responsible for the conversion of angiotensin I (A I) to angiotensin II (A II). This study examined the response of the microvasculature of the hamster cheek pouch to the local application of A I, A II, and the renin substrate, tetradecapeptide (TDP). A I and TDP caused a localized vasoconstriction that was not blocked by converting enzyme inhibitors (CEI: BPF5a for A I and BPF5a and the nonapeptide inhibitor for TDP). However, both the A II antagonist [Sar1, Ala8]angiotensin II and the antiserum to A II blocked completely the A I- and TDP-induced vasoconstriction. Sixty-eight percent of the applied A I was converted to A II in the presence of CEI as well as in its absence. It is concluded that the vasculature of the hamster cheek pouch converts significant amounts of A I to A II by a route that does not involve kininase II.
激肽酶II（血管紧张素I转换酶）通常被认为是负责将血管紧张素I（AI）转化为血管紧张素II（AII）的酶。本研究检测了仓鼠颊囊微血管对局部应用AI、AII和肾素底物十四肽（TDP）的反应。AI和TDP引起局部血管收缩，而这种收缩并未被转换酶抑制剂（CEI：用于AI的BPF5a以及用于TDP的BPF5a和九肽抑制剂）阻断。然而，AII拮抗剂[Sar1，Ala8]血管紧张素II和抗AII抗血清完全阻断了AI和TDP诱导的血管收缩。在有或没有CEI存在的情况下，所应用的AI中有68%被转化为AII。得出的结论是，仓鼠颊囊的血管系统通过一条不涉及激肽酶II的途径将大量AI转化为AII。
