SUMMARY1A change in the arterial pressure‐sympathetic activity or heart rate relation (baroreflex resetting) can result from resetting of baroreceptors (‘peripheral’resetting) or from an altered coupling within the central nervous system of afferent baroreceptor to efferent nerve activities (‘central’resetting).2.‘Peripheral’resetting involves a shift in the pressure‐baroreceptor activity curve in the direction of the prevailing level of arterial pressure, e.g. after elevations in pressure, the baroreceptor pressure threshold (Pth) is increased and activity reduced at equivalent pressures and vascular strains.3.‘Peripheral’resetting occurs during the diastolic phase of a cardiac cycle (instantaneous resetting), after brief exposure to elevated pressure (acute resetting), and during chronic hypertension or when chronic structural changes in the vasculature have occurred (chronic resetting).4Mechanisms include: (i) changes in the mechanical properties of the vessel wall that may alter the tension on the receptors; (ii) ionic mechanisms operating at the neuronal membrane such as activation of Na+, K+‐ATPase; and (iii) release of endothelial factors that may modulate baroreceptor sensitivity.5Acute resetting of baroreceptors can be prevented or attenuated when the sustained elevations in pressure are pulsatile rather than static. Increases in flow increase carotid sinus nerve activity at constant pressure and strain and decrease the Pth of baroreceptors.6.‘Central’resetting can involve neural‐humoral interactions or an altered responsiveness of central neurons mediating the baroreflex to changes in afferent baroreceptor activity.7During static pressure, the continuous baroreceptor discharge causes significant‘central’resetting, i.e. sympathetic activity escapes from baroreflex inhibition. In contrast, during pulsatile pressure, the pulse phasic baroreceptor discharge minimizes‘central’resetting causi