The aim of this study was to examine the contribution of the renin angiotensin system to the antinatriuresis that follows acute volume depletion. Four groups of six dogs each were studied. The first group was exposed to saline expansion (8% body weight) (SE). The second group was exposed to acute volume depletion (2% body weight) followed in one hour by saline expansion (AVD). The third and fourth groups were similar but in dogs treated with high doses of captopril (SE + C and AVD + C). Dogs were anesthetized with phenobarbital. Control measurements were made for 30 minutes before and 60 minutes during saline expansion. Glomerular filtration rate (inulin), renal blood flow (para-aminohippuric acid) and mean arterial pressure were similar in the four groups during the experiment. The increase in fractional sodium excretion from the control period to the end of saline expansion was in the SE group from 0.6 +/- 0.2 to 6.4 +/- 1% and in the SE + C group from 1.1 +/- 0.3 to 8.5 +/- 1.3%. In contrast, in the AVD group it only rose from 0.8 +/- 0.2 to 3.5 +/- 0.7% and in the AVD + C group from 1.3 +/- 0.4 to 4.1 +/- 0.6%. Therefore, the increment in sodium excretion during saline expansion was significantly lower in dogs exposed to acute volume depletion, independent of the treatment with captopril. The blunted natriuresis cannot be explained by differences in GFR, RBF or MAP. These results suggest that renin angiotensin system is not the responsible agent of the sodium retention that follows acute volume depletion.