Sympathetic Nervous Control of Blood Pressure

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Abstract
Actorial, 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 The potential influences and mutual reinforcements of various biological “pressor” factors in primary hypertension, among which the neurogenic ones are particularly powerful though also inherently particularly variable in pattern and extent, appear to be so dominant that it is, in a way, more remarkable that 85% to 90% of the population remain normotensive throughout, then the fact that 10% to 15% develop primary hypertension. This implies that some potent and durable, but so far poorly understood, negative feedbacks are at hand in long-term pressure control, where perhaps the interesting renomedullary depressor system of Muirhead may be of great importance. Am J Hypertens 1989;2:103S-111S

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