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This Article Full Text Full Text (PDF) All Versions of this Article: 290/6/F1543    most recent 00392.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Leong, P. K. K. Articles by Yip, K.-P. Search for Related Content PubMed PubMed Citation Articles by Leong, P. K. K. Articles by Yip, K.-P.

Phenol injury-induced hypertension stimulates proximal tubule Na⁺/H⁺ exchanger activity

¹Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California; and ²Department of Physiology and Biophysics, University of South Florida, Tampa, Florida

Submitted 3 October 2005 ; accepted in final form 27 December 2005

Injection of 50 µl 10% phenol into rat renal cortex activates renal sympathetic nerve activity which provokes acute hypertension that persists for weeks. We have previously shown with membrane fractionation that phenol injury caused a redistribution of the main proximal tubule (PT) apical transporter NHE3 (Na⁺/H⁺ exchanger isoform 3) to low density membranes enriched in apical microvilli. The aim of this study was to determine whether phenol injury increases PT apical Na⁺/H⁺ exchanger (NHE) activity. NHE activity was measured in vivo as the initial rate of change in intracellular pH (dpH_i/dt) during luminal Na⁺ removal in PT preloaded with the pH-sensitive fluorescence dye BCECF. Injection of 50 µl 10% phenol increased blood pressure from 113 ± 5.2 to 130 ± 4.6 mmHg without changing glomerular filtration rate or urine output. NHE activity increased 2.6-fold by 70 min after phenol injury. The increase of NHE activity was accompanied with an increase of tubular reabsorption. Total NHE activity/NHE3 protein in cortical brush-border membrane (BBM) vesicles, measured by acridine orange quench and immunoblot, respectively, was unchanged by phenol injury. In conclusion, acute phenol injury provokes coincident increases in PT apical NHE activity, redistribution of NHE3 into low density apical membranes, and hypertension. The increase in NHE activity may contribute to the lack of pressure-diuresis and the maintenance of chronic hypertension in this model.

sympathetic nervous system; sodium/hydrogen exchanger isoform 3; glomerular filtration rate; proximal tubular flow