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1 Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, CA, USA
2 Department of Medicine, Division of Nephrology, 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 cortical injection of phenol provokes sympathetic nervous system (SNS) dependent hypertension within 30 min associated with acute shift of proximal tubule (PT) NHE3 and NaPi2 to the apical microvilli; the hypertension persists for weeks. This study aimed to determine whether PT Na+ transporter redistribution persists chronically, and whether the pool size of Na+ transporters along the nephron is affected. At 5 weeks after 50 µl 10% phenol injection blood pressure was elevated to 154 ± 8 mmHg vs. 113 ± 11 mmHg after saline injection. Renal cortex membranes were fractionated into three windows enriched in: apical brush border (WI), mixed apical and intermicrovillar cleft (WII) and intracellular membranes (WIII). NHE3 relative distribution in these windows, assessed by immunoblots and expressed as % total, remained shifted to apical membranes from intracellular membranes (WI: 25.3 ± 3% in phenol injected vs.12.7 ± 3% in saline injected and WIII: 9.1 ± 1.3% in phenol injected vs. 18.9 ± 3% in saline injected). NaPi2 and DPPIV also remained shifted to WI and alkaline phosphatase activity increased 100.9 ± 29.7% (WI) and 51.4 ± 17.5% (WII) in phenol injected. Na+ transporters'(NHE3, NaPi2, NCC, NKCC, Na,K-ATPase 
1 and 
1, ENaC and subunits) abundance along the nephron were profiled by immunoblots to assess evidence for escape. Only cortical NHE3 was altered, specifically, cortical NHE3 total abundance decreased to 0.56 ± 0.06 in phenol vs. saline injected. The results demonstrate that the acute shift of PT Na+ NHE3 and NaPi2 to the apical microvilli following phenol injury persists for 5 weeks, but in this chronic phase of hypertension there is also a 44% decrease in total NHE3, evidence for an escape mechanism that would counteract the effects of redistributing a larger fraction of NHE3 to the cell surface by normalizing the total amount of NHE3 in apical membranes to baseline levels.
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