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Am J Physiol Renal Physiol 283: F1142-F1150, 2002. First published July 16, 2002; doi:10.1152/ajprenal.00178.2002
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Vol. 283, Issue 5, F1142-F1150, November 2002

Angiotensin II clamp prevents the second step in renal apical NHE3 internalization during acute hypertension

Patrick K. K. Leong1, Li E. Yang1, Niels-Henrik Holstein-Rathlou2, and Alicia A. McDonough1

1 Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California 90089-9142; and 2 Department of Medical Physiology, Division of Renal and Cardiovascular Research, The Panum Institute, University of Copenhagen, DK-2200 Copenhagen, Denmark

Acute hypertension inhibits proximal tubule (PT) sodium reabsorption. The resultant increase in NaCl delivery to the macula densa suppresses renin release. We tested whether the sustained pressure-induced inhibition of PT sodium reabsorption requires a renin-mediated decrease in ANG II levels. Plasma ANG II concentration of anesthesized Sprague-Dawley rats was clamped by simultaneous infusion of the ANG I-converting enzyme inhibitor captopril (12 µg/min) and ANG II (20 ng · kg-1 · min-1). Blood pressure was increased 50 mmHg for 20 min by arterial constriction ± ANG II clamp or by sham operation. This acute hypertension increased urine output and endogenous Li+ clearance, and these responses were blunted 40-50% in ANG II clamped rats. Acute hypertension provoked a rapid redistribution of Na+/H+ exchanger isoform 3 (NHE3) out of apical brush-border membranes (21 ± 4% decrease of total NHE3 abundance) to endosomal/lysosomal membranes (16 ± 6% increase of total). In ANG II-clamped rats, acute hypertension also provoked disappearance of NHE3 from the apical membranes (27 ± 2% decrease of total), but NHE3 was shifted to membranes enriched in intermicrovillar cleft and dense apical tubules (step 1) rather than endosomal/lysosomal membranes (step 2). This difference was independently confirmed by confocal analysis. In contrast, the pressure-induced redistribution of Na+-Pi cotransporter type 2 was not altered by ANG II clamp. We conclude that the responses to acute hypertension, including diuresis and redistribution of PT NHE3 into intracellular membranes, require a responsive renin-angiotensin system and that the responses may be induced by the sustained increase in NaCl delivery to the macula densa during acute hypertension.

kidney; tubuloglomerular feedback; sodium transport; blood pressure; sodium-phosphate cotransporter type 2


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