The effect of type 1 angiotensin II receptor antagonist treatment (losartan) on cardiac baroreflex regulation of renal sympathetic nerve activity (RSNA) and renal sodium handling in rats with nephrotic syndrome was examined. After intravenous losartan administration, with arterial pressure normalized by intravenous methoxamine, basal RSNA was decreased 14 ± 3% in arterial baroreceptor-intact rats and by 21 ± 5% in arterial baroreceptor-denervated rats. Intracerebroventricular losartan, which did not affect arterial pressure, decreased basal RSNA activity by 15 ± 1%. Both intravenous and intracerebroventricular losartan augmented the renal sympathoinhibitory response to acute volume loading, and this was associated with an enhanced natriuretic response to the acute volume load. In nephrotic syndrome, acute losartan administration improved cardiac baroreflex regulation of RSNA, which was associated with improved ability to excrete acute sodium loads.