5-HT_1A-receptor agonists rapidly restore blood pressure and sympathetic activity in conscious rats subjected to hypotensive hemorrhage. 5-HT_1A-receptor activation has also been shown to produce a robust increase in baroreceptor-dependent, pulse synchronous firing of cardiac sympathetic nerves in anesthetized cats. To determine if 5-HT_1A-receptor agonists reverse hemorrhage-induced suppression of sympathetic activity through facilitation of the arterial baroreflex, the effects of the 5-HT_1A-receptor agonist, 8-OH-DPAT, were assessed in male Sprague-Dawley rats subjected to sinoaortic baroreceptor denervation and subsequent hypotensive hemorrhage. 8-OH-DPAT produced rapid pressor and sympathoexcitatory responses in hemorrhaged animals that were attenuated, but not blocked, by SAD (+49 ± 4 vs. +37 ± 4 mmHg; +165 ±30 vs. +92 ± 24 %baseline, P<0.01). Spectral analysis of sympathetic activity showed that SAD abolished the 8-OH-DPAT-mediated increases in pulse synchronous- (13 ± 1 vs. 5 ± 1 % total power for intact vs. SAD rats, P<0.01) and Mayer wave-related bursting (18 ± 3 vs. 8 ± 1 % total power, P<0.05). However, 8-OH-DPAT continued to increase total power (+72 ± 22 vs. -63 ± 7 %prehemorrhage total power, P<0.05) and power at the respiratory frequency (35 ± 2 % vs. 25 ± 4 %total power) in SAD animals. These data indicate that full expression of the sympathoexcitatory effect of 8-OH-DPAT requires a funtional arterial baroreflex. However, a portion of the effect is due to activation arterial baroreflex-independent sympathetic pathways.