Is bradykinin a mediator of renal neuropeptide Y effects?

Abstract

We have previously reported that the bradykinin receptor antagonist icatibant attenuates the neuropeptide-Y-induced diuresis and natriuresis in anaesthetized rats (Am J Physiol 275:F502-F509, 1998). Therefore, we have now determined whether bradykinin mimics tubular responses to neuropeptide Y in acutely pentobarbital-anaesthetized rats. Infusion of the neuropeptide Y receptor agonist peptide YY (2 micrograms kg-1 min-1) enhanced diuresis and natriuresis approximately equal to 2- and 4-fold, respectively, but did not increase urinary bradykinin excretion. Intrarenal infusion of bradykinin (100 ng kg-1 min-1) reduced renal blood flow by approximately equal to 12% and this was abolished by concomitant administration of icatibant (200 ng kg-1 min-1). However, intrarenal bradykinin infusion did not affect creatinine clearance, urine flow rate or sodium excretion (basal values: 0.8 ml min-1, 111 microliters/15 min and 7.7 mumol/15 min, respectively). These data do not support our original hypothesis that bradykinin mediates the renal effects of neuropeptide Y.