激肽释放酶和激肽可独立刺激分离的大鼠肾小球释放肾素。

Kallikrein and kinins independently stimulate renin release from isolated rat glomeruli.

作者信息

Beierwaltes W H, Carretero O A

出版信息

Adv Exp Med Biol. 1986;198 Pt A:265-72. doi: 10.1007/978-1-4684-5143-6_36.

Abstract

We studied the interaction between kallikrein, kinins, and renin release in isolated rat renal glomeruli and their attendant arterioles. Purified hog kallikrein (170 mEU/ml) significantly stimulated renin release 86% (p less than 0.025) above control. Inactivation of kallikrein by PMSF or inhibition with aprotinin blocked kallikrein stimulation of renin release. Partially purified rat submandibular gland kallikrein (160 mEU/ml) also increased renin by 87% (p less than 0.025). Superfusion of glomeruli with bradykinin (10(-5) M) significantly increased renin release by 108% (p less than 0.025), and lys-bradykinin (10(-5) M) similarly increased renin by 155% (p less than 0.025). Neither of the kinin analogues, des-arg9 bradykinin or tyr8 bradykinin (at 10(-5) M), were able to alter renin released from isolated glomeruli. The vasodilator acetylcholine (10(-5) M) had no effect upon renin release from glomeruli. No kininogen could be detected in glomeruli. Kallikrein superfusion did not result in any measurable kinin generation. We could not detect inactive renin in superfusate or glomeruli after renin activation with either kallikrein or trypsin. These results suggest that kallikrein stimulates renin release independent of kininogenase activity and that this stimulation does not appear to be due to activation of inactive renin. Further, we find that kinins can directly stimulate renin release.

摘要

我们研究了激肽释放酶、激肽与肾素释放之间在分离的大鼠肾小球及其附属小动脉中的相互作用。纯化的猪激肽释放酶（170 mEU/ml）使肾素释放显著增加，比对照高86%（p<0.025）。苯甲基磺酰氟（PMSF）使激肽释放酶失活或抑肽酶抑制均能阻断激肽释放酶对肾素释放的刺激作用。部分纯化的大鼠颌下腺激肽释放酶（160 mEU/ml）也使肾素增加了87%（p<0.025）。用缓激肽（10⁻⁵ M）灌注肾小球显著使肾素释放增加108%（p<0.025），赖氨酰缓激肽（10⁻⁵ M）同样使肾素增加了155%（p<0.025）。两种激肽类似物，去-精氨酸⁹缓激肽或酪氨酰⁸缓激肽（10⁻⁵ M）均不能改变从分离的肾小球释放的肾素。血管扩张剂乙酰胆碱（10⁻⁵ M）对肾小球肾素释放无影响。在肾小球中未检测到激肽原。激肽释放酶灌注未导致任何可测量的激肽生成。在用激肽释放酶或胰蛋白酶激活肾素后，我们在灌注液或肾小球中未检测到无活性肾素。这些结果表明，激肽释放酶刺激肾素释放与激肽原酶活性无关，且这种刺激似乎不是由于无活性肾素的激活。此外，我们发现激肽可直接刺激肾素释放。