| Full text | |
| Author(s): |
Luciano Ramos
[1]
;
Rodrigo Labat
[2]
;
Flávio Aimbire S. Carvalho
[3]
;
Airton Brandão Martin
[4]
;
Rodrigo Álvaro B. Lopes-Martins
[5]
Total Authors: 5
|
| Affiliation: | [1] Universidade do Vale do Paraíba. Programa de Pós-Graduação em Ciências Biológicas - Brasil
[2] Universidade de São Paulo. Instituto de Ciências Biomédicas. Departamento de Farmacologia - Brasil
[3] Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento - Brasil
[4] Universidade do Vale do Paraíba. Instituto de Pesquisa e Desenvolvimento - Brasil
[5] Universidade de São Paulo. Instituto de Ciências Biomédicas. Departamento de Farmacologia - Brasil
Total Affiliations: 5
|
| Document type: | Journal article |
| Source: | Revista Brasileira de Medicina do Esporte; v. 12, n. 4, p. 169-174, 2006-08-00. |
| Abstract | |
It has been clearly established that chronic inhibition of nitric oxide synthesis results in a sustained increase in blood pressure, cardiac remodeling and fibrosis. It was also demonstrated by our group that arginine supplementation was able to increase the skeletal muscle resistance to fatigue, but its mechanism remains uncertain. The experimental treatment of rats with L-NAME is one of the most common models employed to induce hypertension. The expected compensatory response against increases in systemic vascular resistance would be ventricular hypertrophy. However, the presence of cardiac hypertrophy still controversial. The aim of the present study was to verify the effects of nitric oxide inhibition through oral L-NAME administration on the cardiac tissue of rats, and the possible reversion by L-arginine. Thirty male Wistar rats (250-350 g) were kept in controlled conditions of temperature, light, humidity, with water and food "ad libitum". At the end of 4 weeks or treatments the animals were sacrificed by CO2 inhalation and the hearts were removed. Soon after, the hearts were dissected, to separate atria and ventricules, obtaining the total heart weight. After the retreat of the right ventricule, the remaining part was weighed, to obtain the left ventricular weight (LVW, mg); the difference between the total heart weight and the LVW was considered the right ventricular weight (RVW, mg). These values were corrected in function of the corporal weight obtained in the last week of treatment. L-NAME was able to induced hypertension and increases in double product but without any heart hypertrophy. The increase arterial pressure and double product were reversed by L-arginine administration in a dose-dependent way. Preliminary findings demonstrated a reversion of heart fibroses induced by L-NAME, after arginine treatment. We concluded that arginine may constitute a valuable tool in preventing hypertension and cardiac remodeling mainly related to vascular dysfunctions and maybe also in athletic activities. (AU) | |