INHIBITION OF THE KALLIKREIN-KININ SYSTEM AND VASCULAR REACTIVITY IN BARTTERS-SYNDROME

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dc.contributor.authorRODRIGUEZPORTALES, JA
dc.contributor.authorLOPEZMORENO, JM
dc.contributor.authorMAHANA, D
dc.date.accessioned2025-01-23T19:27:41Z
dc.date.available2025-01-23T19:27:41Z
dc.date.issued1985
dc.description.abstractTo study the significance of the increased activity of the kallikrein-kinin system described in patients with Bartter''s syndrome, we investigated the pressor response to infused angiotensin II in four patients with the syndrome receiving no treatment and during the administration of aprotinin and of indomethacin. Five normal subjects served as controls. Aprotinin is a proteolytic enzyme that inhibits the formation of kinins by inhibiting plasma and glandular kallikrein. Indomethacin, a prostaglandin-synthesis inhibitor, can also inhibit the kallikrein-kinin system and normalizes vascular responsiveness to angiotensin II in Bartter''s syndrome. All patients had increased urinary kallikrein and prostaglandin E2 concentrations. Aprotinin significantly decreased the dose of infused angiotensin II required to induce a 20 mm Hg increase in diastolic blood pressure, from 11 .+-. 4 ng/kg per min to 7.0 .+-. 2.0 ng/kg per min (mean .+-. SD; p < 0.05) in normal subjects and from 135 .+-. 57 ng/kg per min to 70 .+-. 26 ng/kg per min (p < 0.05) in the patients with Bartter''s syndrome, without significantly changing plasma renin activity, mean control blood pressure, or urinary prostaglandin E2 concentration. Indomethacin normalized the pressor response to angiotensin II in three patients who had been pretreated for 4 days (pressor dose, 10 ng/kg per min) but not in one patient who received a single oral dose of indomethacin 5 hours before the test. Our results suggest that inhibition of the kallikrein-kinin system alone accounts for approximately a 50% decrease in vascular resistance to the pressor effect of angiotensin II in Bartter''s syndrome, while additional suppression of prostaglandins entirely normalizes the vascular response to angiotensin II. These observations underscore the importance of the kallikrein-kinin system as a vasodilator in Bartter''s syndrome and support the concept that this system may contribute to the regulation of blood pressure in human beings.
dc.fuente.origenWOS
dc.identifier.eissn1524-4563
dc.identifier.issn0194-911X
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/99755
dc.identifier.wosidWOS:A1985AWL2400024
dc.issue.numero6
dc.language.isoen
dc.pagina.final1022
dc.pagina.inicio1017
dc.revistaHypertension
dc.rightsacceso restringido
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleINHIBITION OF THE KALLIKREIN-KININ SYSTEM AND VASCULAR REACTIVITY IN BARTTERS-SYNDROME
dc.typeartículo
dc.volumen7
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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