A model of sympathetic transmission is described in which the capacity of sympathetic nerves to maintain transmitter liberation under various stresses is dependent on rapid regulatory mechanisms such as mobilization of stores, acceleration of synthesis, and reuptake of transmitter, as well as upon long-term changes involving enzyme and vesicle synthesis and transport. Transmitter lost by overflow or metabolism in nerve and muscle is replenished by synthesis, which occurs throughout the neurone but mainly in the axon terminals. Axoplasmic transport of noradrenaline makes little quantitative contribution to stores but reflects the peripheral movement of precursor vesicles concerned with noradrenaline synthesis, storage, and release. These vesicles have a life span of weeks in the axon terminals and repeatedly turn over their noradrenaline stores, which are compartmented. The vesicles contain proteins immunologically identical to those in adrenal medullary vesicles, but the functions of these chromogranins is not known. Like the adrenal, sympathetic nerves release some of their vesicle proteins during transmission, indicating that the mechanism of release of catecholamines is by exocytosis of the contents of the vesicle, total in the adrenal and perhaps partial in nerves. Potential hypertensive mechanisms arising from a disordered life cycle of the vesicles are considered.
|Issue number||4 (Supplement 1)|
|Publication status||Published - Oct 1970|