Modulation of oxidative stress by enalapril and valsartan in adrenaline treated rats: a comparative study

Abstract

Angiotensin (Ang II) II is known to promote oxidative stress in acute myocardial infarction (AMI). Inhibition of renin angiotensin system (RAS) or blockade of Ang II receptors may therefore be effective in reducing oxidative stress during AMI. The study evaluates and compares the protective effect of Angiotensin Converting Enzyme (ACE) inhibitor and AT 1 receptor blocker in adrenaline induced oxidative stress in rats. Rats were treated with two successive injections of adrenaline subcutaneously at a dose of 2 mg/kg administered 24 hours apart. In other two groups of rats enalapril (30 mg/kg) or valsartan (30 mg/kg) were given orally once daily through intragastric tube for 2 weeks and then two injections of adrenaline were administered 24 hours apart. Serum Aspertate Transaminase (AST), plasma Malonde Aldehyde (MDA), erythrocyte GSH and serum vitamin E levels were measured 24 hours after the 2 nd injection of adrenaline in all the groups. Administration of adrenaline caused significant increase (p<0.001) in serum AST and plasma MDA levels and decrease (p<0.001) in erythrocyte GSH and serum vitamin E levels. Pre-treatment of enalapril or valsartan for 14 days reduced (p<0.001) serum AST and plasma MDA levels and increased the concentration of erythrocyte GSH in enalapril pre-treated group (p<0.01) and in valsartan pre-treated group (p<0.05). Pre-treatment of enalapril or valsartan also increased (p<0.01) serum vitamin E levels in adrenaline treated rats. However, no significant difference was noted between the effect of enalapril and valsartan on serum AST, plasma MDA, erythrocyte GSH and serum vitamin E levels. It may be concluded that both enalapril and valsartan offered cardioprotection in adrenaline induced oxidative stress, but the protection afforded by valsartan was not superior to enalapril.

Antioxidant defence and oxidative stress markers in cats with asymptomatic and symptomatic hypertrophic cardiomyopathy: a pilot study

“…It has been found that numerous drugs used to treat hypertrophic cardiomyopathy, such as ACE inhibitors, beta-blockers and calcium channel blockers, may have antioxidant effects [54][55][56]. Contrary to our expectations, we did not find statistically significant differences in any of the oxidative stress parameters between cats without treatment and those in the course of pharmacological therapy.…”

Impact of high-fat diet and hypoxia on the serum levels of main vasoconstrictors in male rabbits

“…This represents a pivotal role of adrenal central part in activating sympathetic system. 9 Although there is no known mechanism to relate central part of adrenal to hypoxia, some publications pointed that the central part of the adrenal is stimulated by hypoxia which subsequently increases the blood catecholamines. 22 A study performed on dogs by Favier et al showed that norepinephrine increased during hypoxia, but there was no increase in epinephrine levels, 23 which was different with our results for epinephrine.…”

“…8 Some researchers have suggested that angiotensin has a direct effect on vascular wall through an intracellular mechanism. 9 Unlike the known effects of angiotensin in atherosclerosis development, effects of catecholamines are different in ischemic and normal conditions. 10,11 Activity of vasoconstrictor system increases following hypoxia in order to increase the cardiac output and compensate the oxygen deficiency.…”

Effect of angiotensin-converting enzyme inhibitor, lisinopril on morphological and biochemical aspects of fibrotic liver regeneration

“…[3536] They can reduce plasma malondialdehyde and increase erythrocyte glutathione content in rats. [37] The decreased lipid peroxidative stress by ACE inhibitors may result in the structural integrity of hepatocytes, thus improving the overall liver function.…”