The adrenaline-synthesizing enzyme PNMT was identified in the early 1970s within a subset of brainstem catecholaminergic neurons thereafter called the C neuronal groups. Since then, most attention has been paid to the C1 group, which resides within the ventrolateral medulla oblongata. In the 1980s, the location of the C1 neurons was shown to coincide with the postulated vasomotor center. Single-unit recordings and neuroanatomical experiments carried out during the same decade strongly suggested that, under anesthesia, the C1 cells drive sympathetic preganglionic neurons monosynaptically and mediate much of the baroreflex. Neurophysiological and anatomical work also revealed that there must be different subgroups of C1 cells and that bulbospinal non-catecholaminergic neurons intermingled with the C1 cells also contribute to BP regulation. An organotopic pattern was proposed whereby subsets of these bulbospinal neurons (C1 or non-C1) would control anatomically defined components of the cardiovascular system (e.g. heart, splanchnic, skin or skeletal muscle beds). In addition to catecholamines, the C1 neurons store and presumably release many neuropeptides. The signaling function of these molecules, catecholamines included, remains elusive in the absence of electrophysiological evidence. Also, the presence of such peptides does not clearly correlate with currently defined functional subclasses of C1 cells. Evidence that C1 cells use glutamate as fast ionotropic transmitter is more compelling. Initially made on the basis of pharmacological data, this suggestion was strengthened by evidence that the C1 neurons of the rat, contrary to the noradrenergic neurons, express vesicular glutamate transporter 2 (VGLUT2). Definitive electrophysiological evidence for release of glutamate by the C1 cells will be presented. Because of their spinal projections, the C1 neurons have too often been viewed as merely “presympathetic” i.e. simple relays of the so-called trisynaptic pathway of the sympathetic baroreflex. This is not the case. Electrophysiological evidence gathered more than 20 years ago already indicated that the vast majority of bulbospinal C1 neurons also project elsewhere in the brainstem and recent comprehensive maps of the projections of the C1 neurons in rodents using viral vectors have revealed how massive their supraspinal projections really are. The function of these projections is now being investigated by several groups using opto- or pharmacogenetics, methods that enable one to selectively enhance or reduce the activity of the C1 neurons including in conscious animals. These experiments have confirmed the expected contribution of the C1 cells to BP control and highlighted their contribution to the central pressor effect of angiotensin II. These methods have also revealed many additional effects of the C1 neurons that are consistent with their wide projection pattern and will be a focus of the talk. For example, the C1 neurons regulate both divisions of the ANS by the most direct route i.e. monosynaptic inputs to the dorsal motor nucleus of the vagus and the SPGNs. They innervate every group of CNS noradrenergic neurons and have a proven excitatory influence on two of them, the locus coeruleus and the A5 neurons. Finally, they regulate breathing and promote arousal. In sum, the C1 neurons could be viewed as the emergency medical technicians (EMTs) of the body, orchestrating autonomic responses designed to cope with acute stresses such as hemorrhage, infection, hypoxia, pain and injury. These responses include adaptive changes in vigilance, vascular resistance, breathing, metabolism (e.g. glucose release), renal function (water preservation), temperature control and immune function and are mediated by both divisions of the ANS and by the pituitary adrenal axis. This spectrum of effects suggests that a contribution of the C1 cells to chronic diseases manifested by simultaneous metabolic, sleep and cardiovascular dysfunction should probably be investigated.