Abstract
We reported that vascular function in adenine-induced renal injury rats was impaired mediated by increase in plasma indoxyl sulfate concentration. It is known that hyperphosphatemia leads to calcification and atherosclerosis. In the present study, we examined effect of hyperphosphatemia on vascular dysfunction in adenine-induced renal injury in anesthetized rats. Renal injury was induced by feeding 0.75% adenine diet for 4 weeks. Lanthanum carbonate was treated with gavage after 2 weeks induced adenine. Treatment with lanthanum carbonate significantly decreased in plasma phosphorus concentration in adenine rats. N-nitro-L-arginine (L-NA) potentiated the ACh-induced depressor response in normal-diet. However, L-NA failed to potentiate the response in adenine rats or lanthanum-treated rats. Sodium nitroprusside (SNP)-induced depressor response in adenine rats was significantly smaller than that in normal rats. Lanthanum carbonate tended to recover impairment of SNP-induced depressor responses in adenine rats. These findings suggest that hyperphosphatemia is partially related to impairment of smooth muscle function rather than that of endothelial function in adenine rats.
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