Angiotensin I-converting enzyme gene polymorphism influences chronic hypertensive response in the rat Goldblatt model

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dc.catalogadorvzp
dc.contributor.authorOcaranza Jeraldino, María Paz
dc.contributor.authorPiddo, Ana M.
dc.contributor.authorFaundez, Perla
dc.contributor.authorLavandero, Sergio
dc.contributor.authorJalil Milad, Jorge Emilio
dc.date.accessioned2024-06-04T16:56:32Z
dc.date.available2024-06-04T16:56:32Z
dc.date.issued2002
dc.description.abstractBackground and objective In humans, the insertion/ deletion polymorphism in the anglotensin (Ang) I converting enzyme (ACE) gene significantly determines ACE activity. The deletion allele induces higher ACE levels and is associated with hypertension in men. In the rat, a microsatellite marker in the ACE gene allows differentiation of the ACE alleles among strains with different ACE levels. We evaluated the effect of genetically determined ACE expression on the development of renovascular hypertension in the rat.
dc.description.abstractMethods and results Systolic BP (SBP), ACE and angiotensin 11 (Ang 11) levels were measured using the Goldblatt (Gb) model (two kidneys, one clip) in homozygous males of two inbred strains (F-2) Of Lewis x Brown-Norway (BN) rats. SBP was significantly higher in the BN-Gb rats compared to the Lewis-Gb rats throughout the study (F = 239.6, P < 0.001). An interaction was observed between SBP and strain (F = 2.92, P < 0.01). Plasma ACE activity was 100% higher in the BN-Gb than in the Lewis-Gb rats (P < 0.05). Ang 11 plasma levels were higher in the BN-sharn than in the Lewis-sham rats (255 +/- 22 versus 161 +/- 16 pg/ml, P < 0.05), increased in both Gb groups and correlated significantly with SBP (r = 0.58, P < 0.01).
dc.description.abstractConclusions Genetically determined ACE expression in male rats enhances the chronic hypertensive response after the induction of renovascular hypertension. A relationship between circulating Ang II and the development of hypertension was also observed in this experimental model of genetically modulated hypertension. (C) 2002 Lippincott Williams Wilkins.
dc.format.extent8 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1097/00004872-200203000-00016
dc.identifier.eissn1473-5598
dc.identifier.issn0263-6352
dc.identifier.pubmedidMEDLINE:11875308
dc.identifier.urihttps://doi.org/10.1097/00004872-200203000-00016
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/86394
dc.identifier.wosidWOS:000174397300016
dc.information.autorucEscuela de Medicina; Ocaranza Jeraldino, María Paz; 0000-0002-4915-6378; 1001254
dc.information.autorucEscuela de Medicina; Jalil Milad, Jorge Emilio; 0000-0001-6877-2072; 99946
dc.issue.numero3
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final420
dc.pagina.inicio413
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.revistaJournal of Hypertension
dc.rightsacceso restringido
dc.subjectAngiotensin
dc.subjectAngiotensin I-converting enzyme
dc.subjectGenetics
dc.subjectHypertension
dc.subjectBrown-Norway rat
dc.subjectLewis rat
dc.subjectGoldblatt model
dc.subjectLEFT-VENTRICULAR MASS
dc.subjectINSERTION DELETION POLYMORPHISM
dc.subjectBLOOD-PRESSURE
dc.subjectACE GENE
dc.subjectRENOVASCULAR HYPERTENSION
dc.subjectRISK FACTOR
dc.subjectPLASMA
dc.subjectLINKAGE
dc.subjectMEN
dc.subjectHYPERTROPHY
dc.subject.ddc610
dc.subject.deweyMedicina y salud
dc.titleAngiotensin I-converting enzyme gene polymorphism influences chronic hypertensive response in the rat Goldblatt model
dc.typeartículo
dc.volumen20
sipa.codpersvinculados1001254
sipa.codpersvinculados99946
sipa.trazabilidadWOS;05-06-2021
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