Effect of Ramipril on Endothelin-1 Expression in Myocardial Tissue at Wistar Rats Induced Myocardial Infarction

Abstract

BACKGROUND: Acute myocardial infarction occurs due to a sudden decrease in coronary blood flow caused by coronary artery embolism, coronary dissection, or coronary vasospasm. The Endothelin-1 (ET-1) is the most potent endogenous vasoconstrictor; it is synthesized and released from vascular and endocardial endothelial cells and myocytes. The action of ET-1 induces endothelial dysfunction in the coronary circulation through several mechanisms, such as reduced NO pathway activity, increased oxidative stress and inflammation, and interference with glucose and lipid metabolism. Ramipril is one of the angiotensin-converting enzyme inhibitors (ACE-I) that can reduce the formation of ET-1 by enhancing the NO expression. NO can down-regulate the ET-1 secretion through soluble guanylate cyclase activation and increased cellular generation of cGMP. AIM: This study aimed to investigate the effect of Ramipril on ET-1 expression in rats-induced myocardial infarction. METHODS: Six-week-old male Wistar rats were randomly allocated into three groups: negative control, positive control was given NaCl 0.9% and treatment group treated with ramipril 3 mg/kg/day orally for 7 days. Myocardial infarction was induced in positive and treatment group by subcutaneous injection of isoproterenol, and 24 h after the last administration, rats were sacrificed to evaluate the relative expression of ET-1 using the real-time polymerase chain reaction and 2-ΔΔCt method. RESULTS: The average expression for the negative control was 0.0098, positive control was 0.0136 and treatment group was 0.0118, with p = 0.210 (p > 0.05). CONCLUSION: Our data suggest that there is no difference between groups for the relative expression of ET-1.