Mechanisms of Renal Injury Induced Chronic Hypertension

Li E. Yang, S. H. Ye, P. K.K. Leong, V.M. Campese, A. A. McDonough
Department of Physiology and Biophysics
University of Southern California, Keck School of Medicine
Los Angeles, CA 90089-9142

Results

Results 1
NHE3 and NaPi2 shifted from intracellular pools (WIII) to apical membranes (WI) 5 weeks after phenol injection

Results 2
No evidence for NHE3 internalization during chronic phase of hypertension induced by phenol injury

Results 3
5 weeks after phenol injection

Results 4
Profiling of Na+ transporter abundance in sham vs chronic phenol - linearity testing of major Na+ transporters

Results 5
Total NHE3 abundance decreased by 42% in cortex 5 weeks after phenol injection

Conclusions

Redistribution of NHE3 and NaPi2 to apical microvilli may contribute to the persistent hypertension induced by phenol injury, suggesting a persistent signal to traffic Na+ transporters to surface.

The decrease in total NHE3, not NaPi2 abundance may be an escape mechanism to normalize ECF salt and water balance. No evidence for "escape" regulation beyond the proximal tubule.