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Articles in PresS, published online ahead of print September 11, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00134.2002
Submitted on April 10, 2002
Accepted on September 10, 2002
1 Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, CA, USA
2 Division of Nephrology, Department of Medicine, University of Southern California Keck School of Medicine, Los Angeles, CA, USA
* To whom correspondence should be addressed. E-mail: mcdonoug{at}hsc.usc.edu.
Renal injury induced by phenol injection activates renal sympathetic afferent pathways, increases norepinephrine release from the posterior hypothalamus, activates renal efferent pathways and provokes a rapid and persistent hypertension. This study aimed to determine whether phenol injury provoked a redistribution of proximal sodium transporters from internal stores to the apical cell surface mediated by sympathetic activation, a response which could contribute to generation or maintenance of hypertension. Anesthetized rats were canulated for arterial blood pressure tracing and saline infusion then 50 µl 10% phenol or saline was injection into one renal cortex (n=7 each). 50 min after injection, kidneys were removed and renal cortex membranes from injected kidneys were fractionated on sorbitol gradients and pooled into 3 windows (W) that contained: enriched apical brush border (WI), mixed apical, intermicrovillar cleft and dense apical tubules (WII) and intracellular membranes (WIII). Sodium transporter distributions were determined by immunoblot and expressed as % total in gradient. Acute phenol injury increased blood pressure 20-30 mmHg, and led to redistribution of NHE3 out of WIII (from 22.79 ± 4.75 to 10.79 ± 2.01% of total) to WI (13.07 ± 1.97 to 27.15 ± 4.08%), NaPi2 out of WII (68.72 ± 1.95% to 59.76 ± 2.21%) into WI (9.5 ± 1.62% to 18.7 ± 1.45%), and a similar realignment of di peptidyl peptidase IV immunoreactivity and alkaline phosphatase activity to WI. Renal denervation prior to phenol injection prevented the NHE3 redistribution. By confocal microscopy NHE3 localized to the brush border after phenol injection. The results indicate that phenol injury provokes redistribution of sodium transporters from intermicrovillar cleft/intracellular membrane pools to apical membranes associated with sympathetic nervous system activation which may contribute to phenol injury induced hypertension.
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