Abstract. Vascular dysfunctions in chronic kidney disease (CKD) include endothelial dysfunctions
and vascular calcification (VC). In the present study, we examined the possible protective effect
of nicorandil (potassium channel opener) on renal and vascular dysfunctions in a rat model of
adenine-induced nephropathy and its underlying mechanisms. Thirty-four male Sprague-Dawley
rats were randomly allocated into 3 groups: Control group, Adenine group (animals received
high-adenine diet for 4 weeks), and Nicorandil group (animals received adenine for 4 weeks and
nicorandil 1 mg/kg per oral for 4 weeks). The results showed significant reduction in the body
weight, heart rate (HR), hemoglobin contents, serum Ca2+ and reduction in the expression of
mRNA of endothelial nitric oxide synthase (eNOS) and nuclear factor erythroid related factor
2 (nrf2) genes in aortic tissues with significant increase in arterial blood pressure (ABP), serum
creatinine, blood urea nitrogen (BUN), plasma renin activity (PRA), K+ and phosphate (PO4
3-),
urinary albumin excretion (UAE) and aortic VC in Adenine group compared to normal group
(p < 0.05). On the other hand, coadminsitration of nicorandil caused significant improvement
in the studied parameters compared to Adenine group (p < 0.05). We concluded that nicorandil
has a potential protective effect against the vascular and renal impairment induced by adenine,
which might be due to attenuation of vascular calcifications, activation of Nrf2 and eNOS genes
in aortic tissues. |
