EVIDENCE FOR RENAL KININS AS MEDIATORS OF AMINO-ACID INDUCED HYPERPERFUSION AND HYPERFILTRATION IN THE RAT

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dc.contributor.authorJAFFA, AA
dc.contributor.authorVIO, CP
dc.contributor.authorSILVA, RH
dc.contributor.authorVAVREK, RJ
dc.contributor.authorSTEWART, JM
dc.contributor.authorRUST, PF
dc.contributor.authorMAYFIELD, RK
dc.date.accessioned2025-01-23T19:22:09Z
dc.date.available2025-01-23T19:22:09Z
dc.date.issued1992
dc.description.abstractThis study examined the role of tissue kallikrein and kinins in renal vasodilation produced by infusion of amino acids (AA). In rats fed a 9% protein diet for 2 wk, intravenous infusion of a 10% AA solution over 60-90 min reduced total renal vascular resistance and increased glomerular filtration rate (GFR) by 25-40% and renal plasma flow (RPF) by 23-30% from baseline. This was associated with a two- to threefold increase in urinary kinin excretion rate. Acute treatment of rats with aprotinin, a kallikrein inhibitor, resulted in deposition of immunoreactive aprotinin in kallikrein-containing connecting tubule cells and inhibited renal kallikrein activity by 90%. Aprotinin pretreatment abolished the rise in urinary kinins and prevented significant increases in GFR and RPF in response to AA. In a second group of rats pretreated with a B2 kinin receptor antagonist, [DArg Hyp3, Thi5.8 D Phe7] bradykinin, AA infusion raised urinary kinins identically as in untreated controls, but GFR and RPF responses were absent. Aprotinin or the kinin antagonist produced no consistent change in renal function in rats that were not infused with AA.AA-induced increases in kinins were not associated with an increase in renal kallikrein activity. Notably, tissue active kallikrein level fell 50% in AA-infused rats. These studies provide evidence that kinins generated in the kidney participate in mediating renal vasodilation during acute infusion of AA.
dc.fuente.origenWOS
dc.identifier.issn0021-9738
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/98976
dc.identifier.wosidWOS:A1992HT98300013
dc.issue.numero5
dc.language.isoen
dc.pagina.final1468
dc.pagina.inicio1460
dc.revistaJournal of clinical investigation
dc.rightsacceso restringido
dc.subjectRENAL FUNCTION
dc.subjectTISSUE KALLIKREIN
dc.subjectDIETARY PROTEIN
dc.subjectKALLIKREIN INHIBITOR
dc.subjectKININ ANTAGONIST
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleEVIDENCE FOR RENAL KININS AS MEDIATORS OF AMINO-ACID INDUCED HYPERPERFUSION AND HYPERFILTRATION IN THE RAT
dc.typeartículo
dc.volumen89
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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