Vasculoprotective effect of cilostazol in aldosterone-induced hypertensive rats


Cilostazol (CILO), a selective inhibitor of phosphodiesterase 3 with potent antithrombotic property, has been shown to have a vasculoprotective effect in atherosclerosis animal models due to its potential anti-inflammatory and antioxidant actions. This study was undertaken to investigate whether CILO has in fact any vasculoprotective effects in aldosterone-induced hypertensive rats (Aldo-rats), and whether CILO affects Aldo-induced oxidative stress, nitric oxide (NO) production and pro-inflammatory gene expression. Treatment with CILO markedly ameliorated perivascular inflammatory changes in the coronary arterioles of Aldo-rats without affecting the systolic blood pressure and left ventricular weight. Treatment with CILO also prevented the increase in plasma levels of thiobarbituric acid-reactive substances, an oxidative stress marker, as well as decreased urinary NOx excretion in Aldo-rats. Furthermore, CILO almost completely inhibited a set of upregulated proinflammatory genes (ICAM-1, MCP-1, PDGF-A, osteopontin, MMP-2 and ACE), as well as NAD(P)H oxidase components (p22phox, gp91phox, p47phox) and Aldo-inducible genes (SGK-1 and NHE-1) in the aortic tissues from Aldo-rats. Taken together, this study showed for the first time that CILO prevented Aldo-induced vascular inflammation and injury without affecting the blood pressure, suggesting its vasculoprotective effect on Aldo-induced vascular injury independent of blood pressure.

DOI: 10.1038/hr.2009.211

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@article{Sakurada2010VasculoprotectiveEO, title={Vasculoprotective effect of cilostazol in aldosterone-induced hypertensive rats}, author={Maya Sakurada and Takanobu Yoshimoto and Naoko Sekizawa and Yuki Hirono and Noriko Suzuki and Yukio Hirata}, journal={Hypertension Research}, year={2010}, volume={33}, pages={229-235} }