The Autonomic Nervous System and Hypertension

That hypertension is due to a derangement of sympathetic and parasympathetic cardiovascular regulation is one of the most widely accredited and tested hypotheses in cardiovascular research. Its proposal followed from the demonstration that autonomic cardiovascular influences play a fundamental role in homeostatic control of the cardiovascular system. In animal models of hypertension, both an increased sympathetic nerve activity and a reduction of vagal cardiac tone are associated with and responsible for the appearance and maintenance of high blood pressure, with their role expanding to include hypertension-related sequelae. Albeit through a longer and more difficult journey, evidence is now available that similar autonomic alterations may have a causative or cocausative role also in the generation and maintenance of human hypertension. We begin this review by describing the alterations in autonomic cardiovascular control that characterize human hypertension. We then discuss the possible mechanisms underlying these alterations and the evidence that they contribute to the functional and structural changes of the heart and systemic circulation that accompany a chronic hypertensive state and lead to its clinical complications. Finally, we consider the effects of nonpharmacological and pharmacological treatment of hypertension on autonomic cardiovascular control. Our focus is limited to the condition defined as essential or primary hypertension, with no reference to the secondary forms of high blood pressure because secondary hypertension accounts for only a small fraction of the overall prevalence of hypertension and its causes do not include alterations of central or reflex autonomic drive. In addition, the concomitant alterations of sympathetic and parasympathetic cardiovascular control that develop in secondary hypertension have been less extensively documented and remain somewhat controversial.