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The effect of enalapril and verapamil on the left ventricular hypertrophy and the left ventricular cardiomyocyte numerical density in rats submitted to nitric oxide inhibition
Author(s) -
Pereira Leila Maria Meirelles,
MandarimdeLacerda Carlos Alberto
Publication year - 2001
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/j.1365-2613.2001.iep172.x
Subject(s) - verapamil , enalapril , medicine , left ventricular hypertrophy , nitric oxide , muscle hypertrophy , cardiology , endocrinology , blood pressure , chemistry , angiotensin converting enzyme , calcium
Forty male Wistar rats were separated into four groups of ten rats each (control and other three groups that have received nitric oxide (NO) synthesis inhibitor L‐NAME) but the last two groups have concomitantly received antihypertensive drugs (Enalapril and Verapamil). After 40 days of experimentation, the heart and the ventricles were measured. The optical disector was used for the calculation of numerical density of the cardiomyocytes (Nv[c]). The left ventricular myocytes number (N[c]) was calculated as the product of Nv[c] and the left ventricular myocardium volume (LVMV) that was determined by using the Scherle's method. In the L‐NAME group the blood pressure (BP) had a significant weekly increment. In the enalapril and the verapamil groups, BP increased in the first two weeks, but decreased in the following weeks. The LVMV increased in the L‐NAME rats and decreased in the enalapril and verapamil animals. The Nv[c] and N[c] decreased in the L‐NAME rats but the verapamil and enalapril treatments maintained the Nv[c] close to the control group. In conclusion, the left ventricular hypertrophy and the significant decrease of the left ventricular cardiomyocyte number caused by the NO synthesis inhibition are efficiently prevented with the use of enalapril and verapamil.