&NA;The reflex mechanisms that produce the neurocirculatory adjustments to hemorrhagic hypotension are incompletely understood. The goal of this study was to determine if hemorrhagic hypotension in rats produces differential effects on sympathetic outflow to the adrenal gland and kidney and if the two sympathetic nerve responses are governed by different reflex mechanisms. We performed simultaneous multifiber recordings of adrenal and renal sympathetic nerve activity (SNA) during 8 minutes of sustained hemorrhagic hypotension to a mean arterial pressure of 50 mm Hg in chloralose‐anesthetized Sprague‐Dawley rats with a) baroreceptors intact, b) cervical vagotomy, c) sinoaortic baroreceptor denervation, and d) combined vagotomy plus sinoaortic denervation. During hemorrhagic hypotension in rats with intact baroreceptors, renal SNA decreased by 31±10% (mean±SEM,p<0.05 vs. control) and heart rate decreased from 384±13 to 365±16 beats per minute (p<0.05), but adrenal SNA increased by 69±10% over control (p<0.05). The decreases in renal SNA and heart rate were reversed by cervical vagotomy but not by atropine, which indicates vagal afferent mediation. In contrast, the increases in adrenal SNA during hemorrhage were not affected by vagotomy alone or by sinoaortic denervation alone but were markedly attenuated by combined sinoaortic denervation and vagotomy, which indicates redundancy in the baroreflex control of adrenal SNA. The major new conclusions from this study are 1) that hemorrhagic hypotension in rats produces directionally opposite reflex changes in renal and adrenal SNA with sympathoinhibition in the kidney but sympathoexcitation in the adrenal gland, and 2) that both of these reflex responses are mediated by vagal afferents. Differential reflex control of regional sympathetic outflow by vagal afferents is an important factor in producing a complex and highly differentiated pattern of autonomic response to this form of hypotension. (Circulation Research1989;64:686‐694)