The vasorelaxant effect of simvastatin in isolated aorta from diabetic rats

• Main Authors: Farshad Roghani-Dehkordi, Mehrdad Roghani
• Format: Article
• Language: English
• Published: Vesnu Publications 2016-04-01
• Series: ARYA Atherosclerosis
• Subjects: Simvastatin; Aorta; Diabetes Mellitus
• Online Access: http://arya.mui.ac.ir/index.php/arya/article/view/884
• ISSN: 1735-3955; 2251-6638

<div><p><strong>BACKGROUND:</strong> The increasing incidence of diabetes mellitus (DM) is of great clinical significance. In this study, we aimed to investigate whether exposure of endothelium-intact aortic rings to simvastatin could have a vasorelaxant effect in diabetic rats.</p> <p><strong>METHODS:</strong> For induction of diabetes, streptozotocin (STZ) (60&thinsp;mg/kg, i.p., single dose) was used. After 1 month, the cumulative reaction of isolated endothelium-intact aortic rings was determined to KCl and phenylephrine (PE) in the absence and presence of nitric oxide (NO) synthase inhibitor, i.e., nitro-L-arginine-methyl ester (L-NAME), and prostaglandin synthesis inhibitor, i.e., indomethacin. Meanwhile, the role of extracellular calcium was assessed in this respect.</p> <p><strong>RESULTS:</strong><strong> </strong>At the end of the study, the addition of simvastatin (at a concentration &ge; 10^&minus;5 M) caused a significant concentration-dependent relaxation response of PE-precontracted aortic rings for both control and diabetic groups (at a significant difference of P &lt; 0.050), and this difference did not exist for KCl-precontracted aortic rings. Furthermore, both L-NAME <br /> (100 &micro;M) and indomethacin (10 &micro;M) significantly diminished the vasorelaxant response following simvastatin addition. Meanwhile, there was no statistically significant difference between control and diabetic groups in the absence of extracellular calcium.</p></div> <strong>CONCLUSION:</strong> The results of this study suggest that simvastatin is able to relax PE-precontracted aortic rings isolated from STZ-diabetic rats via modulation of NO- and prostaglandin-dependent signaling and its effect is not via modulation of calcium mobilization from intracellular stores.