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Abbtract. To study the relationship between vasopressin and the renal kallikrein-kinin system we measured the rate of excretion of kinins into the urine of anesthetized rats during conditions of increased and decreased vasopressin level. The excretion of immunoreactive kinins in Brattleboro rats with hereditary diabetes insipidus (DI) (24±3 pg min-' kg-') was lower than in the control Long Evans (LE) rats (182±22 pg min-' kg-'; P < 0.05). The DI rats also exhibited negligible urinary excretion of immunoreactive vasopressin, reduced urine osmolality, and increased urine flow and kininogenase excretion. In LE rats, volume expansion by infusion of 0.45% NaCl-2.5% dextrose to lower vasopressin secretion reduced (P < 0.05) kinin excretion, vasopressin excretion, and urine osmolality to 41, 26, and 15% oftheir respective control values, while increasing (P < 0.05) urine flow and kininogenase excretion. On the other hand, the infusion of 5% NaCl, which promotes vasopressin secretion, increased (P < 0.05) the urinary excretion of kinins and vasopressin to 165 and 396% of control, while increasing (P < 0.05) urine flow and kininogenase excretion. Infusion of vasopressin (1.2 mU/h, intravenous) enhanced (P < 0.05) kinin excretion by two to threefold in DI rats and in LE rats during volume expansion with 0.45% NaCl-2.5% dextrose, while decreasing urine flow and increasing urine osmolality. This study demonstrates that the urinary excretion of immunoreactive kinins varies in relation to the urinary level of vasopressin, irrespective of urine volume and osmolality and of the urinary excretions of sodium and kininogenase. The study suggests a role forReceivedfor publication 1 7August 1983 and in revisedform 7 November 1983. vasopressin in promoting the activity of the renal kallikrein-kinin system in the rat.

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