It has been suggested that nitric oxide (NO) is a key modulator of both baroreceptor and exercise pressor reflex afferent signals processed within the nucleus tractus solitarius (NTS). However, studies investigating the independent effects of NO within the NTS on the function of each reflex have produced inconsistent results. To address these concerns, the effects of microdialyzing 10 mM L-arginine, an NO precursor, and 20 mM N^G-nitro-L-arginine methyl ester hydrochloride (L-NAME), an NO synthase inhibitor, into the NTS on baroreceptor and exercise pressor reflex function were examined in 17 anesthetized cats. Arterial baroreflex regulation of heart rate (HR) was quantified using vasoactive drugs to induce acute changes in mean arterial pressure (MAP). To activate the exercise pressor reflex, static hindlimb contractions were induced by electrically stimulating spinal ventral roots. To isolate the exercise pressor reflex, contractions were repeated after barodenervation. The gain coefficient of the arterial-cardiac baroreflex was significantly different from control (-0.24±0.04 bpm mmHg^-1 after the dialysis of L-arginine (-0.18±0.02 bpm mmHg^-1) and L-NAME (-0.29±0.02 bpm mmHg^-1). In barodenervated animals, the peak MAP response to activation of the exercise pressor reflex (MAP from baseline =39±7 mmHg) was significantly attenuated by the dialysis of L-arginine (MAP from baseline=29±6 mmHg). The results demonstrate that NO within the NTS can modulate both the arterial-cardiac baroreflex and the exercise pressor reflex independently. Collectively, these findings provide a neuroanatomical and chemical basis for the regulation of baroreflex and exercise pressor reflex function within the central nervous system.