In mammals, catecholamine secretion from adrenal chromaffin cells represents an ubiquitous mechanism helping the organism to cope with stress. Once delivered into the blood circulation, epinephrine and norepinephrine exert multiple actions, leading to physiological adjustments enabling the organism to cope with a threat for its survival. While an instantaneous secretion of catecholamines is beneficial, repeated or prolonged stressful situations are detrimental and can initiate many diseases. Adrenal catecholamine secretion relies on a neurogenic command arising from the splanchnic nerve terminals synapsing onto chromaffin cells and a local gap junctional communication. In response to a systemic stress (5 day-cold exposure, male Wistar rats), both cholinergic synaptic transmission and gap junctional coupling are remodeled. The frequency of excitatory postsynaptic events is increased and the respective contribution of alpha3- and alpha9-containing nAChRs to a scholinergic challenge is modified. While alpha9 nAChRs dominantly support acetylcholine-induced current in cold-stressed rats, alpha3 nAChRs are the main contributing channels in unstressed animals. Expression of Cx36 and Cx43 gap junctions between chromaffin cells is upregulated, leading numerous cells to exhibit co-active Ca2+ signals upon nicotinic application. All these functional changes contribute to the increased plasma catecholamine levels in cold-stressed rats. We next examined the plasticity of the stimulus-secretion coupling in rats suffered from arterial hypertension, a stress-related pathology. Upon robust depolarization, chromaffin cells of adult spontaneously hypertensive male rats are less excitable than cells from normotensive rats. Postsynaptic events also undergo remodeling, as evidenced by a reduced frequency in response to a depolarizing challenge and changes in expression of transcripts encoding nAChR subunits. Additionally, gap junction coupling between chromaffin cells is reduced. These changes are associated with a reduced catecholamine secretion evoked by a robust cholinergic stimulation. As such, the adrenal medullary tissue dualistically and accurately adapts the competence of the stimulus-secretion coupling to appropriately manage catecholamine secretion.