Efeito da administração oral de arginina sobre a pressão arterial e parâmetros cardíacos em ratos submetidos ao bloqueio crônico da síntese de óxido nítrico

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 CO 2 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.

Avaliação da pravastatina em ratos infartados normocolesterolêmicos e sua relação com lípides plasmáticos, colesteral e peroxidação lipídica tecidual e função endotelial

“…A hipertensão arterial também faz parte dos fatores de risco para doença aterosclerótica 23 . Considerada um fator de risco primário pode ocorrer em todas as idades e em ambos os sexos, tem origem multifatorial e está associada a um conjunto de fatores metabolicamente interligados (24) .…”