Effect of lisinopril on rat liver tissues in L-NAME induced hypertension model

Abstract

N(G)-Nitro-L-arginine methyl ester hydrochloride (L-NAME) is a non-specific nitric oxide (NO) inhibitor and it has been used to eliminate the role of NO in many studies like animal models for hypertension. In this study, we aimed to investigate whether lisinopril treatment has any biochemical and/or histopathological effect on rat liver tissue in a L-NAME-induced hypertension model. Forty-eight 6-weeks-old male Spraque-Dawley rats were used in the study. The animals used in the study were randomly divided into four equal groups. To induce hypertension, L-NAME was added to drinking water at a concentration of 600 mg/l and each rat was given 75 mg/kg/day of L-NAME for 6 weeks. Tail cuff systolic blood pressure (SBP) was measured at first, third, and sixth weeks. There was a significant difference between the experiment groups and controls. In only lisinopril given and L-NAME plus lisinopril administered groups, each rat was given 10 mg/kg of lisinopril for 6 weeks. At the end of the study, the animals were sacrificed. Blood and tissue samples were collected for biochemical and histopathological analysis. It has been observed that mean NO level was significantly decreased in L-NAME given group (p<0.05). Mean ALT levels were significantly increased in lisinopril and L-NAME plus lisinopril given groups, when compared with the control group (p<0.05). AST levels were in normal range in all groups (p>0.05). Hepatocyte degeneration was prominent in lisinopril given group, whereas mononuclear cell infiltration was significant in L-NAME given groups. Although the beneficial effects in L-NAME-induced hypertension treatment, lisinopril can lead to some unexpected results like hepatocyte degeneration, serum enzyme level elevation, and slight mononuclear cell infiltration.

Effects of a novel ACE inhibitor, 3-(3-thienyl)-L-alanyl-ornithyl-proline, on endothelial vasodilation and hepatotoxicity in L-NAME-induced hypertensive rats

“…Mononuclear cell infiltration in periportal areas and hepatocellular degeneration are common findings associated with hepatotoxicity. 48 In the present study, periportal mononuclear cell infiltration was the only significant histological finding. Moderate mononuclear cell infiltration was observed in the l -NAME group, while higher levels were observed in the l -NAME + captopril group confirming that captopril causes damage to liver tissues.…”

Evaluation of adverse effects of lisinopril and rosuvastatin on hematological and biochemical analytes in wistar rats

“…However, some earlier studies report hepatocyte degeneration and serum liver enzyme elevation after lisinopril treatment. [25]…”

Basic Pharmacology of NG -Nitro – L – Arginine Methyl Ester

“…Also L-NAME treatment increases the pulmonary arterial pressure & the pulmonary vascular resistance [16]. Also L-NAME treatment produces hypertension [17] and this effect could be explained by other ways rather than to be through NO deprivation. These ways occur simultaneously with the effects of L-NAME on the physiological parameter of the heart via NO deprivation like; an inhibition of acetylcholine vasodilatation effect [18], augmentation the effect of alpha adrenoceptor agonist in endotoxintreated rats [19] and increase the activity of the angiotensin converting enzyme in the aorta due to L-NAME treatment [20].…”