REGULATION OF SYMPATHETIC-NERVE ACTIVITY IN MILD HUMAN HYPERTENSION

There is substantial evidence for increased sympathetic nerve activity in young, mildly hypertensive humans. This evidence has been derived mainly from measurement of plasma catecholamines and from responses to adrenergic antagonists and agonists in normotensive and mildly hypertensive subjects. In addition, in recent studies direct measurements of sympathetic nerve activity to the muscle circulation have been obtained by microneurography. These data also indicate that sympathetic nerve activity is increased in young, mildly hypertensive humans. The present paper reviews this work with microneurographic measurements and highlights several concepts. (1) The increases in sympathetic nerve activity to the muscle in mild hypertension are not a result of impairment in the inhibitory influence of arterial baroreceptors; presumably, they reflect a heightened central nervous system sympathetic drive. (2) In the supine position the inhibitory influence of cardiopulmonary baroreceptors on sympathetic nerve activity is increased in mild hypertension. This increase in cardiopulmonary baroreflex control buffers the heightened sympathetic neural drive in mildly hypertensive subjects in the supine position, but withdrawal of this increase during orthostatic stress produces exaggerated reflex sympathetic vasoconstrictor responses to orthostasis in mildly hypertensive subjects. (3) Arterial chemoreceptor reflexes are increased in mildly hypertensive subjects and lead to exaggerated increases in sympathetic nerve activity during hypoxia. (4) There is increasing evidence that two humoral agents, epinephrine and insulin, exert excitatory effects on sympathetic neural outflow, which may contribute to the increased sympathetic activity and arterial pressure in human hypertension. (5) The postexercise decreases in blood pressure that occur in many subjects with mild hypertension are associated with a decrease in sympathetic neural discharge to muscle, suggesting that the postexercise decrease in blood pressure may be mediated in part by inhibition of sympathetic nerve activity.