In summary, a substantial portion of the excitatory drive to vasomotor sympathetic preganglionic neurons originates from reticulospinal tonically active cells located in the RVLM. This interpretation does not exclude the possible contribution of other tonically active bulbospinal or propriospinal inputs in generating the vasomotor outflow but under usual anesthetic conditions it seems that these alternative inputs are simply insufficient to bring the vasomotor preganglionic neurons to their firing threshold. Such may not be the case after plastic rearrangements consecutive to complete spinalization or chronic lesions of large portions of the RVLM have occurred (Cochrane and Nathan, 1987; for review see Schramm, 1986). It is also clear at present that the RVLM is not merely a final common pathway consisting of premotoneurons passively driven by tonic synaptic inputs originating elsewhere. Indeed the existence of a population of reticulospinal neurons with intrinsic pacemaker activity indicates that the RVLM contains at least one major intrinsic source of tonic activity. These neurons may release a glutamate-like substance and are not phenotypically adrenergic. They have no documented projections outside the cord and could subserve a tone-generating function specific to the sympathetic outflow, e.g. providing a background excitatory input to a large number of preganglionic neurons with vasoconstrictor of cardioaccelerator function. Strong anatomical evidence backed by weaker electrophysiological evidence also support the notion that C1 adrenergic neurons may have a vasomotor role and contribute an excitatory drive to preganglionic neurons. This could be mediated via alpha 1-adrenergic receptors or by receptors to substance P or neuropeptide Y. There is no evidence yet that C1 cells might have intrinsic pacemaker activity. The origin of the ongoing activity of many of these cells "in vivo" is therefore unclear and could depend on an excitatory drive from outside the RVLM. One might speculate that because these cells appear to have collateral interactions (PNMT-immunoreactive boutons synapse on C1 cells, Milner et al., 1987), they could play a role in synchronizing the sympathetic vasomotor outflow (an unexplained phenomenon observable even in the absence of baroreceptor input). Because of the large variety of peptides which they contain, another speculative view could be that they make rather specific connections with subsets of preganglionic neurons and therefore might be responsible for the differential control of regional blood flows by the rostral medulla (Dampney and McAllen, 1988). C1 cells are inhibited by low systemic doses of clonidine and therefore may be in part responsible for the hypotensive effect of this drug.(ABSTRACT TRUNCATED AT 400 WORDS)