Inhibition of transmitter release from isolated rabbit kidney by bradykinin.

The effect of kallikrein on the release of norepinephrine has been studied in the isolated perfused rabbit kidney. Kallikrein in the perfusion medium caused an inhibition in the rise of the perfusion pressure induced by periarterial stimulation and in the contraction of rabbit aorta superfused by the venous outflow of the stimulated kidney. On the contrary, kallikrein caused a potentiation in the urine volume induced by periarterial stimulation. Similar findings were obtained when bradykinin was added instead of kallikrein. Kallikrein did not alter the pressure response and rabbit aorta contraction but potentiated the diuretic effects of exogenously administered norepinephrine. Acetyl salicyclic acid when added to the perfusion medium containing kallikrein caused a reversal in all parameters measured in this study. It is concluded that the changes of the effects of periarterial stimulation of the isolated rabbit kidney by kallikrein are mediated through the bradykinin-mediated increased generation of intrarenal prostaglandins.