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Articles in PresS, published online ahead of print January 2, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00294.2001
Submitted on September 18, 2001
Accepted on December 24, 2001
1 Medicine/Nephrology, Indiana University, Indianapolis, IN, USA
2 Medicine/Nephrology, Indiana University, Indianapolis, IN, USA; Pathology, Indiana University, Indianapolis, IN, USA
3 Medicine/Nephrology, Indiana University, Indianapolis, IN, USA; Roudebush VA Medical Center, Indianapolis, IN, USA
* To whom correspondence should be addressed. E-mail: okwon{at}iupui.edu.
Although altered renal vascular reactivity is known to occur after ischemia, the structural basis explaining the phenomenon has not been clarified. To evaluate for structural damage to the renal vasculature in ischemic acute renal failure (ARF), F-actin in the renal vasculature of rat kidneys and cultured vascular smooth muscle cells was examined using confocal fluorescence microscopy. The left renal artery was clamped for 15 minutes or 45 minutes in Sprague Dawley rats. In other experimental groups, 45 minutes of renal arterial clamping was followed by one or three hours of reperfusion. Control kidneys were procured without any preceding interventional procedure. F-actin was labeled with either fluorescein or Texas red conjugated phalloidin. Serial optical sections were collected by confocal microscopy and image volumes were rendered in three dimensions (3D). The degree of cytoskeletal damage in the vasculature was assessed by semiquantitative scoring of the staining for F-actin. Disorganization/disarray of F-actin, reflected by disruption and clumping of the actin filaments, was observed in arteries, arterioles and the vasa rectae of the kidney after ischemia or ischemia-reperfusion. Smooth muscle cells from arteries and arterioles showed significant damage to F-actin after either 15 or 45 minutes of ischemia in a duration-dependent manner. Damage to the actin cytoskeleton, from 45 minutes of ischemia, tended to recover one and three hours after reperfusion. The vasa rectae did not demonstrate significant damage to F-actin after 15 or 45 minute ischemia. However, significant damage to the vasa rectae was manifest 3 hours after the reperfusion following 45 minutes of ischemia. In summary, disorganization/disarray of F-actin in vascular smooth muscle cells of the kidney was observed after ischemia or ischemia-reperfusion. A similar finding was observed in cultured vascular smooth muscle cells. We suggest that this disorganization of the actin cytoskeleton may play a contributory role to the loss of autoregulation of renal blood flow and the aberrant vascular reactivity in postischemic ARF.
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