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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 · min1). 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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