Vascular effects of kinins in trout and bradykinin metabolism by perfused gill.
Vascular effects of kinins in trout and bradykinin metabolism by perfused gill.
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鳟鱼中激肽的血管效应和灌注鳃的缓激肽代谢。
DOI：
10.1152/ajpregu.1990.258.2.r515
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Olson,KR
中科院分区：
文献类型：
--
作者：
Lipke,DW;Oparil,S;Olson,KR
在前面的研究中，我们已经证明鳟鱼中存在激肽释放酶-激肽系统（KKS）的元素。本研究探讨了动脉内注射激肽对心血管的影响，以及灌注的鳃或鳃匀浆代谢缓激肽或腺激肽释放酶（T60K）在鳟鱼血浆中产生的升压物质的能力。缓激肽 (BK)、t-激肽、激肽和蛋氨酸激肽在体内产生升压反应。 BK 反应不受 α-肾上腺素能阻断或环氧合酶抑制的影响。灌注的鳃提取了大约 40% 的 [3H]BK 丸剂，但是，没有从流出的灌注液中回收代谢物。鳃匀浆完全代谢[3H]BK并使升压物质T60K失活。卡托普利通过鳃匀浆降低 BK 和 T60K 代谢。本研究表明，激肽对鳟鱼具有升压作用，这种作用不是通过肾上腺素能或前列腺素衍生机制介导的。结果还表明，鳟鱼不会因注射激肽而释放内皮衍生的松弛因子。鳃能够代谢 BK 和 T60K，尽管对于 BK，该过程似乎涉及细胞内水解，并且可能仅部分依赖于血管紧张素转换酶。鳃组织对 BK 的灭活可能与哺乳动物肺部的激肽代谢有根本不同。
In the preceding studies we have shown that elements of a kallikrein-kinin system (KKS) are present in trout. The present study examines the cardiovascular effects of intra-arterial kinin injection and the ability of perfused gills or gill homogenates to metabolize bradykinin or the pressor substance generated in trout plasma by glandular kallikrein (T60K). Bradykinin (BK), t-kinin, kallidin, and Met-kallidin produced pressor responses in vivo. BK responses were unaffected by alpha-adrenergic blockade or cyclooxygenase inhibition. Perfused gills extracted approximately 40% of a [3H]BK bolus, however, metabolites were not recovered from the effluent perfusate. Gill homogenates completely metabolized [3H]BK and inactivated the pressor substance T60K. Captopril reduced BK and T60K metabolism by gill homogenates. The present study demonstrates that kinins have pressor effects in trout that are not mediated through adrenergic or prostanoid-derived mechanisms. The results also suggest that trout do not release endothelium-derived relaxing factors in response to kinin injection. The gill is able to metabolize BK and T60K, although, with respect to BK, this process appears to involve intracellular hydrolysis and may be only partially dependent on angiotensin-converting enzyme. Inactivation of BK by gill tissue may be fundamentally different from kinin metabolism by the mammalian lung.