Active and inactive kallikrein were measured along the rabbit microdissected nephron. A sensitive and specific micromethod for the measurement of kininogenase activity was developed in order to quantify kallikrein in pieces of tubule as small as 0.3–0.5 mm. Our study confirms that active and inactive kallikrein are located to the connecting tubule (CNT).

The effects on renal kallikrein of a chronic DOCA treatment and of adrenalectomy were studied. Urinary excretion of kallikrein was also monitored. After DOCA treatment, active kallikrein increased in the tubule and in urine but inactive kallikrein did not significantly change. Adrenalectomy decreased by 50% active and inactive contents of CNT, as well as reduced the excretion of total kallikrein. Kallikrein content in CNT was also measured in adrenalectomized rabbits 3 h after a single injection of either aldosterone (10 μg) or dexamethasone (100 μg). After either aldosterone or dexamethasone injections, kallikrein activities were not restored, whereas in the same animals Na−K-ATPase activity which was depressed on cortical and medullary collecting tubules after adrenalectomy returned toward normal values. These data indicate that kallikrein synthesis and activation are influenced by adrenal hormones. Renal kallikrein is, however, regulated at a much slower rate than Na⁺-K⁺-ATPase. This may suggest an indirect rather than direct action of corticosteroid hormones on kallikrein.