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Citation Information: J Clin Invest. 1980;66(4):757-762. https://doi.org/10.1172/JCI109913.
Abstract
To study the effect of kallikrein on renal renin release, we superfused rat renal cortical slices with 3.5 to 140 milliesterase units (mEU)/ml of purified rat urinary kallikrein. Kallikrein was a potent stimulus of renin release. Renin rose in a dose-dependent fashion from 70 mEU/ml to 140 mEU/ml. The response to 140 mEU/ml was greater than that seen with maximal doses of prostaglandin E2 (170 +/- 43%, P < 0.05) and at least the same as isoproterenol (242 +/- 49% increase), or dibutyryl cyclic AMP (272 +/- 40%). Trypsin was ineffective under these experimental conditions. Kallikrein-stimulated renin release was completely abolished by trasylol, whereas bradykinin did not increase renin production, indicating that kallikrein's effect is not mediated via kinin generation. There was no demonstrable acid activation or kallikrein activation of the superfusate and chromatography on Sephacryl S-200 revealed a single renin peak of -40,000 mol wt, suggesting that all of the renin release was in the active form. The data suggests that urinary kallikrein acts directly on the rat kidney to release renin, possibly via proteolytic conversion of prorenin to active renin. Our results support the concept that kallikrein may be an endogenous activator of prorenin in the kidney.
Authors
S Suzuki, R Franco-Saenz, S Y Tan, P J Mulrow
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