Neurons in the commissural nucleus of the solitary tract (commNTS) play an important role in certain cardiovascular responses dependent on sympathetic vasoconstrictor activation, including the arterial chemoreceptor reflex. Electrolytic lesions of the commNTS elicit a fall in arterial pressure (AP) in spontaneously hypertensive rats (SHR). To determine whether the latter result 1) arose from elimination of commNTS neuronal activity rather than en passant axons and 2) was accompanied by a reduction in sympathetic nerve activity, we evaluated the effect of inhibition of neurons in the commNTS on basal splanchnic sympathetic nerve activity (SNA), AP, and heart rate (HR) in SHR, Wistar-Kyoto (WKY), and Sprague-Dawley (SD) rats. In chloralose-anesthetized, paralyzed, and artificially ventilated SHR, microinjection of GABA into the commNTS markedly decreased splanchnic SNA, AP, and HR. The reductions in SNA and AP following similar microinjections in WKY and SD rats were significantly less than those in SHR. Our findings suggest that tonically active neurons in the commNTS contribute to the maintenance of SNA and the hypertension in SHR. The level of tonic discharge of these commNTS neurons in normotensive WKY and SD rats may be lower than in SHR. sympathetic nerve activity; spontaneously hypertensive rats; ␥-aminobutyric acid; chemoreceptor reflex THE NUCLEUS OF THE SOLITARY TRACT (NTS) is the initial synaptic integration site for baroreceptor and arterial chemoreceptor afferent inputs (5, 9, 39). Baroreceptor afferent activation elicits depressor responses via a sympathoinhibitory pathway from the dorsomedial NTS that involves activation of GABAergic neurons (1,17,18,20,40) in the caudal ventrolateral medulla (CVLM) (2, 12, 22) that inhibit vasoconstrictor sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM). Stimulation of arterial chemoreceptors evokes pressor responses via a sympathoexcitatory pathway from the commissural NTS (commNTS) that excites vasoconstrictor sympathetic premotor neurons in the RVLM either directly (21) or through brain stem pathways that involve neurons in the A5 region (13). Although their relationship to the chemoreceptor reflex is not known, the presence of sympathoexcitatory neurons in commNTS has been suggested by: 1) the increase in arterial pressure (AP) elicited by microinjection of glutamate into commNTS (8,26,31) and 2) the ability of inhibition of commNTS neurons to block both afferent stimulation-evoked increases in AP (24) and those evoked by inhibition of neurons in the CVLM (30).Although electrolytic lesions in commNTS abolish the pressor response evoked by stimulation of the arterial chemoreceptor reflex with potassium cyanide in both normotensive rats and spontaneously hypertensive rats (SHR) (6, 37), it was only in SHR that such lesions reduced the level of basal AP. These data raise the possibility that a tonically elevated level of discharge of commNTS neurons in SHR contributes to the maintenance of hypertension in this model. In the present study, w...