CARDIAC MYOCYTE NECROSIS INDUCED BY ANGIOTENSIN-II

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dc.contributor.authorTAN, LB
dc.contributor.authorJALIL, JE
dc.contributor.authorPICK, R
dc.contributor.authorJANICKI, JS
dc.contributor.authorWEBER, KT
dc.date.accessioned2024-01-10T13:46:34Z
dc.date.available2024-01-10T13:46:34Z
dc.date.issued1991
dc.description.abstractAlthough the role of angiotensin II (Ang II) in the pathogenesis and progression of the failing heart is uncertain, previous reports have suggested that myocyte injury may be a component in this process. In this study, we investigated this possibility in more detail. Cardiotoxic effects of nonacutely hypertensive doses of Ang II were examined in 90 rats, including those receiving an angiotensin infusion (200 ng/min i.p.) and those with renovascular hypertension, where endogenous stimulation of Ang II occurred. Myocyte injury and wound healing resulting from these treatments were evaluated by 1) immunofluorescence after in vivo monoclonal antibody labeling of myosin to detect abnormal sarcolemmal permeability, 2) [H-3]thymidine incorporation into DNA, to detect fibroblast proliferation, and 3) light microscopic evidence of myocytolysis and subsequent scar formation. We found that exogenous Ang II produced multifocal antimyosin labeling of cardiac myocytes and myocytolysis, which were maximal on days 1-2 of the infusion. Subsequently, DNA synthesis rates were increased, with fibroblast proliferation reaching peak levels on day 2 (Ang II-treated rats, 90.0 +/- 18.6 cpm/mu-g DNA; control rats, 11.4 +/- 2.3 cpm/mu-g DNA; p < 0.05); microscopic scarring was found on day 14 and represented 0.12 +/- 0.02% of the myocardium. Concurrent treatment with both propranolol (30 mg/kg/day s.c.) and phenoxybenzamine (5 mg/kg/day i.m.) did not attenuate Ang II-induced antimyosin labeling. Increased endogenous Ang II, resulting from renal ischemia after abdominal aortic constriction, produced both antimyosin labeling and increased rates of DNA synthesis like that observed with Ang II infusion. Both myocyte injury and fibroplasia were prevented with captopril (65 mg/day p.o.), but this protective effect was not seen with reserpine pretreatment. Infrarenal aortic banding without renal ischemia, on the other hand, produced hypertension without necrosis. We conclude that pathophysiological levels of endogenous as well as low-dose exogenous Ang II were associated with altered sarcolemmal permeability and myocytolysis with subsequent fibroblast proliferation and scar formation. Myocyte injury was unrelated to the hypertensive or enhanced adrenergic effects of Ang II or to hypertension per se. Captopril was effective in preventing myocyte injury in renovascular hypertension. The mechanism(s) responsible for Ang II-induced necrosis will require further study.
dc.description.funderNHLBI NIH HHS
dc.description.funderNATIONAL HEART, LUNG, AND BLOOD INSTITUTE
dc.fechaingreso.objetodigital2024-05-16
dc.format.extent11 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1161/01.RES.69.5.1185
dc.identifier.eissn1524-4571
dc.identifier.issn0009-7330
dc.identifier.pubmedidMEDLINE:1834362
dc.identifier.urihttps://doi.org/10.1161/01.RES.69.5.1185
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/79175
dc.identifier.wosidWOS:A1991GN52100002
dc.information.autorucMedicina;Jalil J;S/I;99946
dc.issue.numero5
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final1195
dc.pagina.inicio1185
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.revistaCIRCULATION RESEARCH
dc.rightsacceso restringido
dc.subjectMONOCLONAL ANTIMYOSIN
dc.subjectRENOVASCULAR HYPERTENSION
dc.subjectCAPTOPRIL
dc.subjectMYOCARDIAL FIBROSIS
dc.subjectCONGESTIVE HEART-FAILURE
dc.subjectRAT CORONARY-ARTERIES
dc.subjectVASCULAR-PERMEABILITY
dc.subjectINDUCED HYPERTENSION
dc.subjectBLOOD-PRESSURE
dc.subjectMYOCARDIUM
dc.subjectNOREPINEPHRINE
dc.subjectPLASMA
dc.subjectRABBIT
dc.subjectEPINEPHRINE
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleCARDIAC MYOCYTE NECROSIS INDUCED BY ANGIOTENSIN-II
dc.typeartículo
dc.volumen69
sipa.codpersvinculados99946
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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