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1 Departments of Pediatrics and 2 Internal Medicine, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235-9063
In the present study, we examined whether the effect of
endogenously produced angiotensin II on proximal tubule transport in
the male Sprague-Dawley rat is regulated by acute changes in extracellular volume. We measured the magnitude of endogenous angiotensin II-mediated stimulation of transport by sequentially perfusing proximal tubules in vivo, first with an ultrafiltrate-like solution, then by reperfusion of the same tubule with an
ultrafiltrate-like solution containing
10
8 M losartan (angiotensin
II receptor antagonist). During volume contraction,
108 M losartan decreased
volume reabsorption from 4.20 ± 0.50 to 1.70 ± 0.30 nl · mm1 · min1
(P < 0.05), a decrease of 58.0 ± 7.0%. In contrast, after acute volume expansion,
108 M losartan decreased
volume reabsorption from 1.84 ± 0.20 to 1.31 ± 0.20 nl · mm1 · min1
(P < 0.05), a decrease of 29.6 ± 9.0%. In hydropenic rats, addition of exogenous luminal angiotensin II
had no effect on transport. However, in volume-expanded rats, addition
of 108 M angiotensin II
increased volume reabsorption from 2.10 ± 0.34 to 4.38 ± 0.59 nl · mm1 · min1
(P < 0.005). These data are
consistent with endogenously produced angiotensin II augmenting
proximal tubule transport to a greater degree during volume contraction
than after volume expansion.
autocrine; losartan; microperfusion; kidney
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