Polarity of kallikrein release and activation in perfused rat kidneys

The polarity of release and activation of renal kallikrein and its regulation by adrenal hormones was studied in isolated perfused rat kidneys. Bilateral adrenalectomy (AX) produced a decrease in kallikrein and prokallikrein excretion into urine and perfusate of isolated kidneys, as well as in active kallikrein excretion in vivo. One-week treatment with deoxycorticosterone acetate (DOCA 2.5 mg/day) or dexamethasone (DEX 0.25 mg/day) increased the urinary output of active and total kallikrein above AX levels but below control. In contrast, neither corticoid increased enzyme secretion to perfusate. Regardless of AX or corticosteroid treatment, the prokallikrein fraction was 90% of total enzyme in perfusate and only 40% in urine. These results confirm that adrenal steroids are necessary for renal kallikrein synthesis and excretion; however, neither DOCA nor DEX appears to be a unique regulator for release or activation of this enzyme. In addition, whereas the processes of secretion and activation toward the urine are regulated in parallel, kallikrein release to the venous effluent seems to be regulated separately.