Rho kinase activation and gene expression related to vascular remodeling in normotensive rats with high angiotensin I-converting enzyme levels

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dc.catalogadoraba
dc.contributor.authorRivera, Paulina
dc.contributor.authorOcaranza, María Paz
dc.contributor.authorLavandero, Sergio
dc.contributor.authorJalil Milad, Jorge
dc.date.accessioned2024-06-10T21:25:28Z
dc.date.available2024-06-10T21:25:28Z
dc.date.issued2007
dc.description.abstractThe RhoA/Rho kinase (ROCK) pathway is a new mechanism of remodeling and vasoconstriction. Few data are available regarding ROCK activation when angiotensin I-converting enzyme is high and blood pressure is normal. We hypothesized that ROCK is activated in the vascular wall in normotensive rats with genetically high angiotensin I converting enzyme levels, and it causes increased vascular expression of genes promoting vascular remodeling and also oxidative stress. Aortic ROCK activation, mRNA and protein levels (of monocyte chemoattractant protein-1, transforming growth factor [TGF]-beta(1), and plasminogen activator inhibitor-1 [PAI-1]), NADPH oxidase activity, and O-2(.-) production were measured in normotensive rats with genetically high (Brown Norway [BN]) and low (Lewis) angiotensin-I-converting enzyme levels and in BN rats treated with the ROCK antagonist fasudil (100 mg/kg per day) for 7 days. ROCK activation was 12-fold higher in BN versus Lewis rats (P<0.05) and was reduced with fasudil by 100% (P<0.05). Aortic TGF-beta 1, PAI-1, and monocyte chemoattractant protein-1 mRNA levels were higher in BN versus Lewis rats by 300%, 180%, and 1000%, respectively (P<0.05). Aortic TGF-beta 1, PAI-1, and monocyte chemoattractant protein-1 protein levels were higher in BN versus Lewis rats (P<0.05). Fasudil reduced TGF-beta 1 and PAI-1 mRNA and TGF-beta 1, PAI-1, and monocyte chemoattractant protein-1 protein aortic levels to those observed in Lewis rats. Aortic reduced nicotinamide-adenine dinucleotide phosphate oxidase activity and .O-2(-) production were increased by 88% and 300%, respectively, in BN rats (P<0.05) and normalized by fasudil. In conclusion, ROCK is significantly activated in the aortic wall in normotensive rats with genetically high angiotensin-I-converting enzyme and angiotensin II, and it causes activation of genes that promote vascular remodeling and also increases vascular oxidative stress.
dc.description.funderFONDECYT
dc.format.extent7 páginas
dc.fuente.origenHistorial Académico
dc.fuente.origenORCID
dc.identifier.doi10.1161/HYPERTENSIONAHA.107.095117
dc.identifier.issn0194-911X
dc.identifier.urihttps://doi.org/10.1161/HYPERTENSIONAHA.107.095117
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/86687
dc.identifier.wosidWOS:000249586900034
dc.information.autorucEscuela de Medicina; Ocaranza, María Paz; 0000-0002-4915-6378; 1001254
dc.information.autorucEscuela de Medicina; Jalil Milad, Jorge; 0000-0001-6877-2072; 99946
dc.issue.numero4
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final798
dc.pagina.inicio792
dc.revistaHypertension
dc.rightsacceso restringido
dc.subjectRho
dc.subjectAngiotensin-converting enzyme
dc.subjectAngiotensin
dc.subjectRemodeling
dc.subjectFasudil
dc.subjectNADPH
dc.subjectHypertension
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.titleRho kinase activation and gene expression related to vascular remodeling in normotensive rats with high angiotensin I-converting enzyme levels
dc.typeartículo
dc.volumen50
sipa.codpersvinculados1001254
sipa.codpersvinculados99946
sipa.trazabilidadORCID;2024-06-03
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