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, 10-8 M losartan decreased volume reabsorption from 4.20 ± 0.50 to 1.70 ± 0.30 nl · mm-1 · min- 1 (P < 0.05), a decrease of 58.0 ± 7.0%. In contrast, after acute volume expansion, 10-8 M losartan decreased volume reabsorption from 1.84 ± 0.20 to 1.31 ± 0.20 nl·mm-1·min-1 (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 10-8 M angiotensin II increased volume reabsorption from 2.10 ± 0.34 to 4.38 ± 0.59 nl·mm-1· min-1 (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.
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