Recent histochemical and other studies have revealed that renal kallikrein is localized in cells in the connecting tubules of the nephron and that low molecular weight (LMW) kininogen is found in the principal cells in the connecting tubules (Figueroa et al, 1988). These sites are adjacent, and once renal kallikrein and LMW kininogen are secreted, kinin is promptly generated in the tubules. Kallistatin, a tissue kallikrein inhibitor, is also secreted in the collecting ducts of the inner medulla (Chen et al, 1995). Bradykinin B 2 receptors are distributed along the collecting ducts (Figueroa et al, 1995). These observations clearly suggest that the renal kallikrein-kinin system may have some roles to play in the kidney, but its precise roles have not yet been clarified.

We have had an opportunity to study the roles of the renal kallikrein-kinin system using mutant kininogen-deficient Brown Norway-Katholiek (BN-Ka) rats or natural knockout rats (Katori & Majima, 1996). Here, we introduce some recent findings on the roles of the renal kallikrein-kinin system in rats in relation to the development of hypertension. The detailed results have been published in review articles (Majima & Katori, 1995; Katori & Majima, 1996, 1998).