Effect of hypertension on angiotensin-(1-7) levels in rats with different angiotensin-I converting enzyme polymorphism

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dc.contributor.authorOcaranza, MP
dc.contributor.authorPalomera, C
dc.contributor.authorRoman, M
dc.contributor.authorBargetto, J
dc.contributor.authorLavandero, S
dc.contributor.authorJalil, JE
dc.date.accessioned2024-01-10T12:38:30Z
dc.date.available2024-01-10T12:38:30Z
dc.date.issued2006
dc.description.abstractTo determine circulating angiotensin-(1-7) [Ang-(1,7)] levels in rats with different angiotensin converting enzyme (ACE) genotypes and to evaluate the effect of hypertension on levels of this heptapeptide, plasma levels of angiotensin II (Ang II) and Ang-(1-7) were determined by HPLC and radioimmunoassay in (a) normotensive F-0 and F-2 homozygous Brown Norway (BN; with high ACE) or Lewis (with low ACE) rats and (b) in hypertensive F-2 homozygous male rats (Goldblatt model). Genotypes were characterized by PCR and plasma ACE activity measured by fluorimetry. Plasma ACE activity was 2-fold higher (p < 0.05) in homozygous BN compared to homozygous Lewis groups. In the Goldblatt groups, a similar degree of hypertension and left ventricular hypertrophy was observed in rats with both genotypes. Plasma Ang II levels were between 300-400% higher (p < 0.05) in the BN than in the Lewis rats, without increment in the hypertensive animals. Plasma Ang-(1-7) levels were 75-87% lower in the BN rats (p < 0.05) and they were significantly higher(p < 0.05) in the hypertensive rats from both genotypes. Plasma levels of Ang II and Ang-(1-7) levels were inversely correlated in the normotensive rats (r = -0.64; p < 0.001), but not in the hypertensive animals. We conclude that there is an inverse relationship between circulating levels of Ang II and Ang-(1-7) in rats determined by the ACE gene polymorphism. This inverse relation is due to genetically determined higher ACE activity. Besides, plasma levels of Ang-(1-7) increase in renovascular hypertension. (c) 2005 Elsevier Inc. All rights reserved.
dc.fechaingreso.objetodigital01-04-2024
dc.format.extent8 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1016/j.lfs.2005.07.026
dc.identifier.eissn1879-0631
dc.identifier.issn0024-3205
dc.identifier.pubmedidMEDLINE:16229862
dc.identifier.urihttps://doi.org/10.1016/j.lfs.2005.07.026
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/77054
dc.identifier.wosidWOS:000235853100002
dc.information.autorucMedicina;Jalil J;S/I;99946
dc.information.autorucMedicina;Ocaranza M;S/I;1001254
dc.issue.numero14
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final1542
dc.pagina.inicio1535
dc.publisherPERGAMON-ELSEVIER SCIENCE LTD
dc.revistaLIFE SCIENCES
dc.rightsacceso restringido
dc.subjectangiotensin
dc.subjectangiotensin-(1-7)
dc.subjectangiotensin converting enzyme polymorphism
dc.subjecthypertension
dc.subjectINSERTION DELETION POLYMORPHISM
dc.subjectLEFT-VENTRICULAR HYPERTROPHY
dc.subjectGENE POLYMORPHISM
dc.subjectBLOOD-PRESSURE
dc.subjectNEUTRAL ENDOPEPTIDASE
dc.subjectMYOCARDIAL-INFARCTION
dc.subjectACE GENE
dc.subjectPLASMA
dc.subjectBRADYKININ
dc.subjectRENIN
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleEffect of hypertension on angiotensin-(1-7) levels in rats with different angiotensin-I converting enzyme polymorphism
dc.typeartículo
dc.volumen78
sipa.codpersvinculados99946
sipa.codpersvinculados1001254
sipa.indexWOS
sipa.trazabilidadCarga SIPA;09-01-2024
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