The Autonomic Nervous System and Hypertension

Abstract

T hat 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.1-3 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. [4][5][6][7] 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 8 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. 1,4,6 Autonomic Dysfunction in PrehypertensionAbnormal increases in circulating plasma levels of the adrenergic neurotransmitters norepinephrine and epinephrine The Autonomic Nervous System and Hypertension Giuseppe Mancia, Guido GrassiThis Review is in a thematic series on The Autonomic Nervous System and the Cardiovascular System, which includes the following articles:

“Broken” autonomic cardiac circadian clock in obese adolescents: evidence and implications

“…Studies in adult obese patients clearly show that this is the case. Indeed, regular physical exercise has been clearly shown to improve autonomic balance by exerting an inhibition of the sympathetic excitatory effects and, throughout a baroreflex potentiation, a clear-cut reinforcement of vagal cardiac drive [2,17]. Similar results can be achieved by introducing a hypocaloric diet, which may reduce body weight by at least 10 % [18].…”

“…However, when circadian curves of estimated high-frequency components detected in obese and control subjects are compared, it becomes clear that the difference in the two curves is greater for magnitude in the daytime period between 6.00 a.m. and 2.00 p.m. This time window includes the early morning hours known to be associated with a pronounced adrenergic overdrive to the heart and peripheral vessels, and with a greater risk of sudden arrhythmic death, particularly in obese patients [2,7].…”

“…Specifically, the authors performed power spectral analysis of the 24-h heart rate signal in order to determine whether and to what extent the high-frequency/low-frequency components of the R-R interval, which are well known to represent reliable indices of parasympathetic/sympathetic cardiac drive, respectively [2], are altered in these subjects. Data that were analyzed by adjustments for confounders (specifically age and gender) were compared to those obtained in non-obese children and adolescents.…”

“…This is because no relationship exists between the data collected by the power spectral analysis and those obtained via direct measures of sympathetic drive, such as those collected via the microneurographic recording of efferent postganglionic muscle sympathetic nerve traffic in the peroneal nerve [10]. Finally, in the study by Rodriguez-Colon et al [1], information is available on the presence, as well as the severity, of the sleep apnea syndrome in the obese adolescents studied, and thus, on the independent effects, this obesityrelated complication may have on parasympathetic and sympathetic neural function [2,11,12]. The intriguing results of the study by Rodriguez-Colon et al [1] offer the chance to briefly address in the second part of this editorial two relevant practical questions, i.e., (1) why we should care about the study findings and (2) whether the described circadian autonomic abnormalities are irreversible, or if they can be favorably affected by a given therapeutic intervention.…”

“…These include an increase in peripheral vascular resistance, which in conjunction with the sodium retention by the kidney and the reninangiotensin stimulation (both processes being triggered by the adrenergic activation [2]) may favor the development and progression of a blood pressure increase [13]. These also include the metabolic abnormalities, with a particular emphasis on the development and progression of an insulin resistance state which again has a promoting role in the genesis of the sympathetic overdrive [2,8,9,14]. They finally include the development of heart failure and life-threatening cardiac arrhythmias, given again the relevance of the sympathetic overdrive in the pathophysiology of these two frequent cardiovascular complications of the obese state [2,15,16].…”