Chronic nitric oxide inhibition as a model of hypertensive heart muscle disease

dc.creatorMoreno, H
dc.creatorMetze, K
dc.creatorBento, AC
dc.creatorAntunes, E
dc.creatorZatz, R
dc.creatordeNucci, G
dc.date1996
dc.dateMAY-JUN
dc.date2014-12-16T11:32:19Z
dc.date2015-11-26T16:28:05Z
dc.date2014-12-16T11:32:19Z
dc.date2015-11-26T16:28:05Z
dc.date.accessioned2018-03-28T23:09:05Z
dc.date.available2018-03-28T23:09:05Z
dc.identifierBasic Research In Cardiology. Dr Dietrich Steinkopff Verlag, v. 91, n. 3, n. 248, n. 255, 1996.
dc.identifier0300-8428
dc.identifierWOS:A1996UV79400008
dc.identifier10.1007/BF00788911
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/55903
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/55903
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/55903
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1269366
dc.descriptionWe have compared the myocardial alterations in rats made hypertensive by the chronic inhibition of nitric oxide biosynthesis with those having renal hypertension (two kidney-one clip model), Male Wistar rats were chronically administered the nitric oxide synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) for 2, 4 and 8 weeks. Both groups initially developed a similar increase in blood pressure but only the 2K-1C rats developed myocardial hypertrophy after 2-4 weeks. L-NAME-treated animals developed a similar degree of hypertrophy following 8 weeks of treatment, As observed by light microscopy, the myocardial alterations in the latter animals consisted of extensive areas of fibrosis and myocardial necrosis: especially in regions of the subendocardium. The histological alterations induced by L-NAME were not caused by the accompanying hypertension, since the 2K-1C animals had a similar increase in arterial blood pressure without any significant alterations in the heart morphology. 2K-1C rats treated chronically with L-NAME behaved in a manner similar to the L-NAME-treated animals with regard to both the blood pressure increases and cardiac morphological alterations. Animals which received the inactive enantiomer D-NAME did not develop hypertension nor did they have any morphological abnormalities. Both the coronary flow and the contractile capacity of hearts isolated from rats treated viiith L-NAME for 8 weeks were impaired compared to control animals. These results indicate that the chronic inhibition of NO biosynthesis causes cardiac ischemia associated with a mechanical dysfunction that is unrelated to cardiac hypertrophy which is similar to those seen in some patients suffering from chronic arterial hypertension.
dc.description91
dc.description3
dc.description248
dc.description255
dc.languageen
dc.publisherDr Dietrich Steinkopff Verlag
dc.publisherBerlin 33
dc.publisherAlemanha
dc.relationBasic Research In Cardiology
dc.relationBasic Res. Cardiol.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectendothelium
dc.subjectL-NAME
dc.subjectarterial hypertension
dc.subjectleft ventricular hypertrophy
dc.subjectmyocardial ischemia
dc.subjectLeft-ventricular Mass
dc.subjectCoronary Flow
dc.subjectRat
dc.subjectBlockade
dc.subjectHypertrophy
dc.subjectEndothelium
dc.subjectSynthase
dc.subjectPressure
dc.subjectDamage
dc.titleChronic nitric oxide inhibition as a model of hypertensive heart muscle disease
dc.typeArtículos de revistas


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