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

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.