Is bradykinin a mediator of renal neuropeptide Y effects?
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.
Bischoff
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Medizinische Klinik, Universitätsklinikum Essen, Germany.
Neumann
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Dendorfer
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Michel
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MC
D000818:Animals; D001920:Bradykinin / Q000502:physiology* / Q000652:urine; D007262:Infusions, Intravenous; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009478:Neuropeptide Y / Q000494:pharmacology*; D019894:Peptide YY / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
D009478:Neuropeptide Y; D019894:Peptide YY; D001920:Bradykinin