Abstract
Background/Aims: Vasoactive compounds are known to affect intrarenal hemodynamics and gene transcription, but specific effects of fenoldopam in the setting of acute renal ischemia are not known. We utilized a rat model of acute ischemic nephropathy to test the hypothesis that fenoldopam improves corticomedullary tissue oxygen tension (P<sub>t</sub>O<sub>2</sub>) and attenuates angiogenesis gene expression in acute renal ischemia. Methods: Rats anesthetized with 50 mg/kg urethane were divided into 4 groups (n = 6 each): (1) sham with infusion of 0.9% saline; (2) sham with infusion of 0.1 µg·kg<sup>–1</sup>·min<sup>–1</sup> fenoldopam; (3) unilateral renal ischemia followed by 6 h of reperfusion with saline, and (4) ischemia/reperfusion with fenoldopam. Renal artery blood flow (RBF), renal cortical perfusion (RCP), and P<sub>t</sub>O<sub>2</sub> were recorded throughout. Total RNA from left kidneys was used to probe microarrays. Gene expression was measured as percent positive control (GAPDH) and confirmed using RT-PCR. Results: Fenoldopam significantly increased RBF (p < 0.05), RCP (p < 0.01) and P<sub>t</sub>O<sub>2</sub> (p <0.01) in both non-ischemic and post-ischemic kidneys. Fenoldopam attenuated 11 of the 13 ischemia-induced genes and 44 of 78 ischemia-suppressed genes. This attenuation was statistically significant (p <0.05) for five genes. Conclusion: Data from this rat model of ischemic nephropathy suggest that fenoldopam improves intrarenal hemodynamics and attenuates ischemia-related changes in angiogenesis gene expression.
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