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Am J Physiol Renal Physiol 256: F894-F900, 1989;
0363-6127/89 $5.00
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AJP - Renal Physiology, Vol 256, Issue 5 894-F900, Copyright © 1989 by American Physiological Society

ARTICLES

Renal ischemia and reperfusion impair endothelium-dependent vascular relaxation

W. Lieberthal, E. F. Wolf, H. G. Rennke, C. R. Valeri and N. G. Levinsky
Evans Memorial Department of Clinical Research, University Hospital, Boston University Medical Center, Massachusetts.

We studied the hemodynamic response of the isolated erythrocyte-perfused kidney to 25 min of ischemia and found that renal vascular resistance (RVR) was increased in the reflow period (16.7 +/- 1.4 mmHg.ml-1.min.g following ischemia vs. 10.2 +/- 0.8 mmHg.ml-1.min.g in control kidneys). Endothelial independent vasodilators [atrial natriuretic factor (ANF) and sodium nitroprusside] prevented the increase in RVR that occurred after ischemia. In contrast, acetylcholine and the calcium ionophore A23187, two vasodilators that act by releasing endothelium-derived relaxing factor (EDRF), had no effect on the increased RVR that occurs on reflow. Two inhibitors of EDRF, methylene blue and gossypol, increased RVR in nonischemic kidneys by 45 +/- 6 and 46 +/- 11%, respectively, an increase that was comparable to that found with ischemia alone (55 +/- 7%). The increase in RVR found with the combination of EDRF inhibition and ischemia (59 +/- 5%) was the same as that found with ischemia alone. We conclude that EDRF activity is impaired following ischemia and reperfusion. This abnormality in EDRF may be an important mechanism contributing to postischemic vasoconstriction in the renal vasculature.


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