Microinjection of angiotensin II into the nucleus tractus solitarii attenuates the baroreceptor reflex mediated bradycardia by inhibiting both vagal and cardiac sympathetic components. However, it is not known whether the baroreflex modulation of other sympathetic outputs (i.e. non-cardiac) are also inhibited by exogenous Angiotensin II in nucleus tractus solitarii. Here, we determined if there was a difference in the baroreflex sensitivity of sympathetic outflows at the thoracic and lumbar levels of the sympathetic chain following exogenous delivery of angiotensin II into nucleus tractus solitarii. Experiments were performed in two types of in situ arterially perfused decerebrate rat preparations. Sympathetic nerve activity was recorded from the inferior cardiac nerve, the mid-thoracic sympathetic chain or the lower thoracic-lumbar sympathetic chain. Increases in perfusion pressure produced a reflex bradycardia and sympathoinhibition. Microinjection of angiotensin II (500 fmol) into the nucleus tractus solitarii attenuated the reflex bradycardia (57% attenuation, P<0.01) and sympathoinhibition of both the inferior cardiac nerve (26% attenuation, P<0.05) and mid-thoracic sympathetic chain (37% attenuation, P<0.05), but not the lower thoracic-lumbar chain (P=0.56). We conclude that angiotensin II in the nucleus tractus solitarii selectively inhibits baroreflex responses in specific sympathetic outflows, possibly dependent on the target organ innervated.