Conjugates of the toxin saporin (SAP) have been widely used to target select neurons while leaving other neurons undisturbed. Using one such conjugate we found that an antibody to dopamine-β-hydroxylase conjugated with SAP (antiDBH-SAP) killed catecholamine neurons in the nucleus tractus solitarii (NTS) while sparing other neurons. Bilateral injections of anti-DBH-SAP into the NTS led to attenuation of baroreceptor reflexes, lability of arterial pressure, and, in some animals, sudden death. However, targeting the same neurons with 6-hydroxydopamine produced no such cardiovascular events. We hypothesized that the conjugates may target non-neuronal cells in the NTS and found that, indeed, local astrocytes were killed by the conjugates as well as by unconjugated SAP itself. SAP injections into the NTS led to loss of glial fibrillary acidic protein (GFAP). Although there were positive markers for astrocytic death, neuronal structural markers and neuronal biosynthetic enzymes were undisturbed. Our recent studies have further suggested that local neurons are physiologically intact. Nonetheless, SAP injections into the NTS significantly reduced cardiovascular responses elicited by glutamate agonists injected into the NTS. Furthermore, bilateral injections of SAP into the NTS led to attenuation of cardiovascular reflexes whose pathways pass through the NTS, lability of arterial pressure, damage to cardiac myocytes and sudden death resulting from asystole. When asystole and death followed SAP treatment the fatal arrhythmia followed progressive bradycardia. In that treated animals demonstrate altered ventilatory function, we conjecture that it is altered ventilation that leads to cardiac compromise and death.