Relative Preservation of the Responsiveness to Endothelin-1 During Reperfusion Following Renal Ischemia in the Rat

Abstract

Reperfusion after renal ischemia is characterized by a preglomerular vasoconstriction. As endothelin-1 (ET-1) is a potent preglomerular vasoconstrictor, we designed a study to investigate the role of ET-1 in postischemic renal vasoconstriction. Renal ischemia was induced by 45 min of left renal artery clamping in anesthetized rats. After ischemia, renal blood flow was restored to only 61 +/- 4% of its preischemic value. The sensitivity to exogenous ET-1 after renal ischemia was decreased, but much less than the sensitivity to angiotensin II, which almost lost its vasoconstrictor effect, and to norepinephrine, which became a vasodilator. In addition, the binding affinity of [125I]ET-1 in the kidney increased significantly after renal ischemia, despite no change in the density of binding sites. These findings may be in favor of a role of endogenous ET-1 in postischemic renal vasoconstriction.