Innervation of the heart: An invisible grid within a black box

Abstract

Autonomic control of cardiovascular function is mediated by a complex interplay between central, peripheral, and innate cardiac components. This interplay is what mediates the normal cardiovascular response to physiologic and pathologic stressors, including blood pressure, cardiac contractile function, and arrhythmias. However, in order to understand how modern therapies directly affecting autonomic function may be harnessed to treat various cardiovascular disease states requires an intimate understanding of anatomic and physiologic features of the innervation of the heart. Thus, in this review, we focus on defining features of the central, peripheral, and cardiac components of cardiac innervation, how each component may contribute to dysregulation of normal cardiac function in various disease states and how modulation of these components may offer therapeutic options for these diseases.

Ganglionic GFAP+ glial Gq-GPCR signaling enhances heart functions in vivo

“…SNS activation enhances left ventricle contraction (26). We examined whether glial Gq-GPCR activation leads to changes in left ventricular contractility in conscious Gfap-hM3Dq mice using echocardiography.…”

Cardiac Arrhythmia following Stroke

“…To put it simply, a center of the efferent parasympathetic innervation of the heart is found in the nucleus of the medulla oblongata, especially in the nucleus dorsalis [1]. The preganglionic fibers leave the central nervous system along with the vagus nerve and are connected to the second neuron in cardiac ganglion cells.…”

“…In addition, in the blood circulating catecholamine, the release of which in the adrenal system is also subject to the autonomic system, mediates beta-adrenergic effects on the myocardium. It is postulated that dysbalances in the extrinsic system, in particular the pathological disinhibition of sympathetic activity, are relevant to the development of cardiac arrhythmias [1,[3][4][5]. For example, extensive brain stem damage can lead to suppression of central parasympathetic functions and overcoming of sympathetic tone [6], thus promoting the occurrence of cardiac arrhythmias.…”

“…For the control of cardiac functions, the profound part of the plexus cardiacus is decisive; it extends between the tracheal bifurcation and the aortic arch, divides into a right and left half and in its further course follows the right or left coronary artery. The function of the efferent limb is modified by afferents from various organ systems, including the gastrointestinal tract or the carotissinus, by means of multisynaptic reflex arcs (e. g., baroreflex) [1]. In addition, in the blood circulating catecholamine, the release of which in the adrenal system is also subject to the autonomic system, mediates beta-adrenergic effects on the myocardium.…”

Is there such as a thing as non-ischaemic cardiac pain?: Table 1

“…Its activity is most likely mediated by adenosine receptors located on the endings of unmyelinated C fibres 3. As adenosine is typically released when nucleotide triphosphates are depleted, the notion that it is the most significant mediator of cardiac pain is in harmony with the hypothesis that angina is induced whenever myocardial oxygen demand greatly exceeds supply 2.…”