The adrenal medullary tissue plays an important role in blood pressure (BP) regulation through the secretion of catecholamines (CA). In response to chronic stress, the sustained or repetitive rises of plasma CA have deleterious consequences on body homeostasis and are well-known risk factors for hypertension. Increased BP is associated with a sympathetic hyperactivity leading to a raised neural tone and increased plasma CA, thus assigning the sympatho-adrenal axis as a relevant neurogenic component of hypertension. To date, the intra-adrenal mechanisms dedicated to compensate a recurrent high BP remain unknown. We therefore investigated the remodeling of the stimulation-secretion coupling in acute slices in adult spontaneously hypertensive rats (SHRs), by combining electrophysiology, RT-qPCR and HPLC-based CA assays. SHR chromaffin cells exhibit broader and lower-amplitude action potentials, evocative of a reduced excitability, which is especially marked upon robust depolarisations. This is accompanied by changes in the mRNA expression profile of various voltage-gated ion channels. The expression of  and  nicotinic receptor subunit mRNAs also differs between SHRs and normotensive rats and correlates with a reduced frequency of postsynaptic events in response to a high K+ challenge. Morever, the reduction in both Lucifer yellow diffusion between chromaffin cells and connexin43 expression denotes an attenuated gap junctional communication in SHRs. Accordingly, CA secretion, monitored at rest and in response to cholinergic stimulations, is less efficient in SHRs. As such, by reducing its competence to release CA, the hypertensive medulla has elaborated an adaptive protection mechanism against damaging effects of recurrent elevated CA secretion.