Emerging Excitatory Role of Cardiovascular Sympathetic Afferents in Pathophysiological Conditions

Abstract

Abstract-There is sound experimental evidence that cardiovascular sympathetic afferent fibers mediate cardiovascular reflexes largely excitatory in nature with positive-feedback characteristics. This afferent neural channel is likely to normally participate in the neural regulation of cardiovascular function. The hypothesis, which is the core of this article, is that in some pathophysiological conditions, sympathetic overactivity may be partly due to an emerging excitatory reflex action of cardiovascular sympathetic afferents. In fact, the early phase of congestive heart failure can be characterized by an increase in arterial pressure and heart rate and/or by a diastolic dysfunction, leaving unchanged the cardiac output; in these conditions, in which no baroreceptor deactivation should occur, it is possible that cardiovascular sympathetic afferents with sensory endings in the thoracic low-pressure areas, highly responsive to volume loading, are responsible for mediating the reflex sympathetic excitation. Similarly, during acute myocardial infarction, ventricular sympathetic afferents are likely to mediate a reflex sympathetic overactivity, which is known to facilitate sudden death. Finally, numerous reports have described in essential arterial hypertension an increased sympathetic activity that may be due, at least in part, to the reinforcing action of sympathosympathetic reflexes. Thus, in pathophysiological conditions, cardiovascular sympathetic afferents would mediate a reflex sympathetic overactivity independently of baroreceptive mechanisms, and such an absence of a homeostatic purpose would provide a better rationale for some beneficial effects of therapeutic correction. Key Words: heart failure Ⅲ ischemia Ⅲ hypertension, arterial Ⅲ heart rate Ⅲ reflex Ⅲ lung T he present article will attempt to support the hypothesis that in the early phase of congestive heart failure and other pathophysiological conditions, such as myocardial ischemia and arterial hypertension, sympathetic excitation seems devoid of an ultimate homeostatic purpose, and its genesis may be, in part, attributable to an enhanced peripheral excitatory function of sympathetic afferent fibers.In physiological conditions, the cardiovascular neural regulation is likely to result from a complex interaction of central integration and peripheral inhibitory and excitatory reflexes. [1][2][3] In this interplay, cardiovascular sympathetic afferent fibers mediate a reflex action that is largely excitatory in nature 1 (Figure). When a sympathetic excitation is part of an integrated physiological pattern with a clear ultimate purpose, such as emotion, the central neural and, in particular, diencephalic mechanisms 4 are likely to play a predominant role. However, the central command is also likely to be reinforced by a synergistic enhancement of peripheral excitatory reflex mechanisms, accompanied by a simultaneous attenuation of mechanisms exerting an inhibitory action. 3,4

Sympathetic Drive in Anterior and Inferior Uncomplicated Acute Myocardial Infarction

“…However, we found no correlation between sympathetic nerve activity and indices of arterial pressure as previously reported in other clinical conditions, 4,25 supporting the proposal that sympathetic excitation was independent of baroreceptor reflex function. 19 Also, we have previously shown that the sympathetic hyperactivity early after AMI persisted for at least 3 months despite normalization of arterial pressure. 4 With regard to therapy, it has been reported in patients with heart failure that ACE inhibitors decrease sympathetic nerve activity 35 and that ␤-blockers have no effect on MSNA.…”

“…One of the postulated mechanisms of sympathetic activation after acute myocardial ischemia or infarction has involved chemical activation or impairment of sympathetic or vagal afferents, respectively, and their interaction. [17][18][19] There has been experimental evidence showing that sympathetic afferents are evenly distributed throughout the anterior and inferoposterior walls of the left ventricle and that their activation by chemicals or ischemia in any of these locations leads to a similar reflex sympathetic activation. 20 In contrast, the chemosensitive vagal afferents, the excitation of which leads to sympathetic inhibition, are located primarily in the inferoposterior walls of the left ventricle.…”

“…For instance, after the demonstration of a sympatho-sympathetic cardiac reflex, 16 other reports have reported that excitation of left ventricular sympathetic afferents is a significant mechanism leading to sympathetic activation after acute myocardial ischemia and infarction. [17][18][19] These afferents are evenly distributed in the walls of the left ventricle, such that their excitation at any site causes similar reflex efferent sympathetic activation. 20 Indeed, in humans, plasma norepinephrine levels have been reported to increase to a similar extent in patients who sustain either an ant-AMI or inf-AMI.…”

Relação entre a variabilidade da frequência cardíaca e VO 2pico em mulheres ativas

“…Estudos prévios revelaram que as adaptações na modulação autonômica da FC, frente ao treinamento físico, podem ser detectadas de forma não invasiva através da análise linear da variabilidade da FC (VFC) 1,2 . Recentemente, os métodos não lineares têm merecido grande atenção devido à interação de subsistemas que responde a estímulos internos e externos, como comandos central, periférico e humoral, os quais estão envolvidos na gênese da dinâmica da FC 8,9 . Esta metodologia baseou-se no comportamento não linear da FC frente à complexa interação entre estes vários sistemas (sistema nervoso central, mecanismos reflexos e fatores neuro-humorais), os quais fornecem informações adicionais sobre os mecanismos envolvidos na regulação cardiovascular 10,11 .…”

Sympathovagal balance changes in sleep breathing disorders

“…On the other hand parasympathetic activity acts as protective factor against the above mentioned conditions (4). Some studies have recently highlighted the ANS involvement in the inflammatory response and in altering the endothelial function.…”