Sympathetic nervous control of blood pressure. Role in primary hypertension

After a brief historic survey, sympathetic-neurogenic contributions to the multifactorial, polygenetically linked etiology of primary (essential) hypertension are outlined towards the background of experimental findings both in various rat models and in human subjects. It is emphasized how at least some variants of both human and rat primary hypertension show a genetically linked, central nervous system (CNS)-dependent increase of responsiveness to ordinary daily psychosocial stimuli. Such influences, conveyed by way of neurohormonal response patterns, seem to act in concert with cardiovascular structural adaptation, also sometimes genetically reinforced, so as to gradually elevate the pressure equilibrium until a state of "established" hypertension is reached. However, also in variants characterized by, eg, a genetically increased sensitivity to salt intake of renal or other origin, neurohormonal mechanisms seem to be involved early, though probably via other types of central mechanisms, thereby helping to convey the pressure-elevating influences of the altered salt-volume handling. Evidence is now at hand to indicate that these two "environmental factors," ie, excitatory psychosocial influences and increased salt intake, which at least partly operate via different genetic elements, are in fact closely intertwined, and even mutually reinforcing as to their actions. It is also briefly outlined how neurogenic contributions seem to vary in extent and type of impact, not only between different variants of hypertension but also along with the stage of disorder, probably being, in most cases, particularly important in the early stages.(ABSTRACT TRUNCATED AT 250 WORDS)