Impairment of renal organic anion transport mediated by organic anion transporter 1 (Oat1) and 3 (Oat3) in acute myocardial ischemic and reperfusion injury in rats

Abstract

Acute kidney injury (AKI) is frequently associated with acute myocardial infarction (AMI). Kidney plays a crucial role in the clearance of uremic toxins, produced from organ dysfunctions, mainly through organic anion transporters 1 (Oat1) and 3 (Oat3). This study aims to examine the effects of acute myocardial ischemia and ischemic/reperfusion (I/R) on renal transporter functions, and identify the mechanisms involved in the impairment of these transporters. Myocardial ischemia and I/R were induced in rats by either 30‐minute left anterior descending coronary artery occlusion or 30‐minute occlusion followed by 120‐minute of reperfusion, respectively. The renal hemodynamic parameters and renal transporter functions were subsequently determined along with renal biochemical markers. Results showed that myocardial ischemia led to reduction in renal blood flow, perfusion pressure, and kidney function by approximately 40%, while the reperfusion phase partially recovered renal hemodynamic parameters. Moreover, myocardial ischemia and I/R progressively induced renal oxidative stresses and mitochondria dysfunction, all of which directly deteriorated renal Oat1 and Oat3 functions. Thus, this study indicates that myocardial ischemia and I/R conditions leads to a progressively declined renal transport function, which could potentially worsen AKI. Renal Oat1 and Oat3 transporters, therefore, might be potential therapeutic targets for reversing such injury.Support or Funding InformationThis research was supported by the Thailand Research Fund (RSA5980009 to CS), Faculty of Medicine Endowment Fund, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.