Bradykinin effects on adrenergic transmission in the canine kidney: relation to prostaglandins

We studied the action(s) of bradykinin at the renal vascular neuroeffector junction, and its relation to prostaglandin synthesis, by investigating the effect of the peptide on the renal venous output of the neurotransmitter and on the renal vasoconstrictor responses elicited by sympathetic nerve stimulation and by norepinephrine in pentobarbital-anesthetized dogs. Renal arterial infusion of bradykinin at 10 ng . kg-1 . min-1 increased blood flow to the kidney and inhibited the vasoconstrictor effect of renal nerve stimulation (1-8 Hz) and injected norepinephrine (0.06-0.5 micrograms). However, bradykinin did not alter the rise in venous output of norepinephrine elicited by nerve stimulation. Infusion of another vasodilatory peptide, substance P (2 ng . kg-1 . min-1) into the renal artery also increased blood flow to the kidney but failed to alter the vasoconstriction produced by either adrenergic stimulus. Pretreatment of dogs with an inhibitor of prostaglandin synthesis, either sodium meclofenamate or indomethacin (5 mg/kg), abolished the inhibitory effect of the kinin on renal vasoconstriction produced by adrenergic stimuli. These data suggest that bradykinin acts on postjunctional sites to reduce adrenergically induced vasoconstriction in the canine kidney by a mechanism dependent on prostaglandin synthesis.