Brainstem catecholaminergic neurons have been implicated as mediating adaptive autonomic and neuroendocrine responses to cardiovascular challenges. To clarify the nature of this involvement, immuno‐ and hybridization histochemical methods were used to follow c‐fos expression in these neurons in response to acute stimuli that differentially affect blood pressure and volume. From low basal levels, hypotensive hemorrhage (15%) provoked a progressive increase in the number and distribution of Fos‐immunoreactive (ir) nuclei in the nucleus of the solitary tract (NTS), the Al and C1 cell groups of the ventrolateral medulla, and in the pontine A5, locus coeruleus, and lateral parabrachial cell groups peaking at 2.0–2.5 hours after the challenge. Fos‐ir ventrolateral medullary neurons, subsets of which were identified as projecting to the paraventricular hypothalamic nucleus or spinal cord, were predominantly aminergic, whereas most of those in the NTS were not. Infusion of an angiotensin II antagonist blunted hemorrhage‐induced Fos expression in the area postrema, and attenuated that seen elsewhere in the medulla and pons. Nitroprusside‐induced isovolemic hypotension yielded a pattern of c‐fos induction similar to that seen following hemorrhage, except in the area postrema and the Al cell group, where the response was muted or lacking. Phenylephrineinduced hypertension stimulated a restricted pattern of c‐fos expression, largely limited to non‐aminergic neurons, whose distribution in the NTS conformed to the termination patterns of primary baroreceptor afferents, and in the ventrolateral medulla overlapped in part with those of vagal cardiomotor and depressor neurons. These findings underscore the importance of brainstem catecholaminergic neurons in effecting integrated homeostatic responses to cardiovascular challenges and their ability to responding strategically to specific modalities of cardiovascular information. They also foster testable predictions as to effector neuron populations that might be recruited to respond to perturbations in individual circulatory parameters. © 1994 Wiley‐Liss, Inc.