Autonomic Innervation of Specific Organs


The heart receives parasympathetic and sympathetic innervation. The cell bodies of the parasympathetic preganglionic neurons innervating the heart are located in the medulla (nucleus ambiguous and dorsal motor nucleus of the vagus). The axons of these neurons, which are part of the vagus nerve, join the cardiac neural plexus after entering the thorax to synapse with neurons in the intracardiac ganglia. y From these ganglia, short postganglionic parasympathetic neurons emerge to innervate the myocardial tissue. Vagal innervation is particularly abundant in the nodes and the atrioventricular (A-V) conduction system.

The heart draws its sympathetic innervation from neurons in the intermediolateral columns of the spinal cord at the T1-T4 levels. Axons of these neurons synapse in superior, middle, and inferior (stellate) cervical ganglia, which are the origin of postganglionic sympathetic neurons that reach the heart in a mixed neural plexus along with preganglionic parasympathetic neurons. Sympathetic axons innervate the sinoatrial (SA) and atrioventricular (AV) nodes, the conduction system, and myocardial muscle fibers, most prominently in the ventricles. The arteries and veins of the systemic circulation are innervated primarily by the sympathetic system.

Postganglionic parasympathetic neurons release acetylcholine, which activates muscarinic receptors in the heart, causing a decrease in heart rate as well as reductions in the conduction, excitability, and contractility of myocardial cells. Postganglionic sympathetic axons release norepinephrine, which, primarily via beta-adrenergic receptors, increases heart rate and the conduction, excitability, and contractility of the myocardium. Cardiac vagal neurons are activated through the baroreflex (see later discussion) when arterial pressure increases and are inhibited during inspiration. y Because acetylcholine acts quickly and is rapidly inactivated by cholinesterase, the vagus controls heart rate on a beat-to-beat basis.

Sympathetic outflow to the arteries, arterioles, and veins of the peripheral circulation produces vasoconstriction by activating alpha-adrenergic receptors. The presence of vasodilator cholinergic sympathetic fibers to skeletal muscle in humans is debatable. Sympathetic vasoconstrictor outflow to the blood vessels of skeletal muscle is strongly modulated by the baroreflex (see later discussion) and is important for buffering acute changes in arterial pressure.

Splanchnic vasoconstriction produced by sympathetic activation is critical for the maintenance of arterial pressure in the upright posture. Loss of splanchnic vasomotor outflow is the main mechanism causing orthostatic hypotension in autonomic failure.

Autonomic outflow to the heart and blood vessels is controlled on a moment-to-moment basis by a variety of reflexes, which are initiated by arterial baroreceptors and chemoreceptors and by several types of cardiac receptors. Of these reflexes, the one that has been best studied is the arterial baroreflex, which is a classic negative feedback mechanism that buffers fluctuations in arterial blood pressure. Afferent fibers in the vagus and glossopharyngeal nerves with cell bodies in the nodose and petrosal ganglia are sensitive to pressure or mechanical distention (i.e., baroreceptors). These neurons have arborizations that are distributed in the adventitial layer of the carotid sinus and the aortic arch, and their first synapse occurs in the NTS. Impulses from the NTS modify the activity of cardiac vagal motor neurons in the nucleus ambiguus and neurons in the ventrolateral medulla that control sympathetic outflow. y When arterial pressure increases, afferent baroreceptor discharge in the NTS increases. This results in a rapid increase in cardiovagal efferent activity, which slows the heart, and in inhibition of sympathetic vasoconstrictor outflow, which causes vasodilatation. Conversely, when blood pressure falls, for example when standing up, baroreceptors are "unloaded," and their afferent discharge to the NTS decreases. This results in reflex sympathetic excitation and parasympathetic inhibition, which cause vasoconstriction and tachycardia.

Cardiovascular reflexes also control the release of vasopressin from the supraoptic and paraventricular hypothalamic nuclei. These neurons are tonically inhibited by baroreceptor input, and therefore a fall in arterial pressure elicits an increase in vasopressin release. y


Sympathetic innervation of the skin plays an important role in thermoregulation and the expression of emotional states. The sympathetic outflow to the skin includes cholinergic neurons innervating sweat glands (sudomotor neurons) and adrenergic neurons innervating blood vessels and hair follicles (vasoconstrictor and pilomotor neurons). Cutaneous vasomotor activity and sweating in the face is controlled by the T2-T3 segments of the spinal cord via the superior cervical ganglion. Postganglionic axons accompany branches of the internal carotid (for innervation of the forehead) and external carotid arteries (innervating the rest of the face) and follow branches of the trigeminal nerve. Sympathetic outflow produces vasoconstriction in the ears and lips but predominantly vasodilatation in the rest of the face. Fibers from the stellate ganglion (which receives innervation from T2-T6 preganglionic neurons) innervate the arm via branches of the brachial plexus. The lumbar sympathetic ganglia (which receives innervation from T9-L1 preganglionic neurons) innervate the lower limb via branches of the lumbosacral plexus. The trunk is innervated by the intercostal nerves.

Exposure to cold produces skin vasoconstriction (pallor) and piloerection (goose flesh) via alpha-adrenergic mechanisms; conversely, a warm environment elicits vasodilatation (redness, flushing) and sweating via muscarinic receptors. During certain emotional states (fear, anxiety) and hemodynamic stimuli (severe fall in arterial pressure), both vasoconstrictor and sudomotor outputs are activated simultaneously, producing a cold, clammy skin ("cold sweat").


The dorsal nucleus of the vagus innervates the entire gastrointestinal tract with the exception of the proximal esophagus and the distal colon and rectum. The vagus produces increases in propulsive motility, relaxation of sphincters, and secretions of the exocrine and endocrine glands of the stomach, intestine, pancreas, and liver. Sympathetic outflow to the gastrointestinal tract, which arises from preganglionic neurons at the T1-L1 segments of the spinal cord and relays, via the splanchnic nerves, in the celiac and mesenteric ganglia, is involved in reflexes that decrease gut motility. Extrinsic vagal and sympathetic influences are relayed and integrated at the level of the enteric nervous system, located in the wall of the gut.


The function of the bladder, rectum, and sexual organs is controlled by three outflows: sacral parasympathetic, lumbar sympathetic, and somatic. Control of the bladder serves as a paradigm for innervation of the other pelvic organs. The sacral parasympathetic (S2-S4) output to the bladder is carried via the pelvic nerves and is mediated by muscarinic cholinergic receptors. These parasympathetic nerves promote bladder emptying (micturition) through activation of the detrusor muscle and relaxation of the bladder neck. The lumbar sympathetic (T11-L2) output is carried via the hypogastric nerves. The sympathetic nerves produce relaxation of the detrusor muscle by way of beta receptors and contraction of the bladder neck by way of alpha receptors, thus favoring storage of urine. The sacral somatomotor output, which arises from motor neurons of the nucleus of Onuf (S2-S4) and is carried by the pudendal nerve, stimulates contraction of the external sphincter via nicotinic cholinergic receptors. Activation of these somatomotor nerves promotes storage of urine. y

In normal individuals, micturition involves a spino-ponto-spinal reflex that is initiated by bladder tension receptors and integrated in pontine micturition centers. This reflex coordinates the simultaneous activation of sacral parasympathetic autonomic neurons and inhibition of somatic sphincter motor neurons, thus allowing synergistic bladder contraction and sphincter relaxation during micturition. y

Interruption of the sacral parasympathetic outflow in patients with lesions of the conus or cauda equina results in a hypotonic areflexic bladder. In patients with spinal cord lesions the suprasegmental pathway is interrupted, and micturition occurs through segmental spinospinal sacral reflexes, which are triggered by perineal or nociceptive stimulation. In this condition, bladder and sphincter contractions are not well coordinated, resulting in detrusor-sphincter dyssynergia. Cortical inputs are responsible for

voluntary control of initiation and interruption of micturition. Lesions involving the medial aspects of the frontal lobes, including the anterior cingulate and paracentral gyri, result in involuntary but coordinated micturition, referred to as uninhibited bladder.


Autonomic innervation of the pupil (see Chapter.9 ) and the lacrimal and salivary glands (see C.,h..apt,e.r 1.,.1.. and Ch.apte.L13.) is reviewed in the chapters discussing the specific cranial nerves controlling these structures.


Relaxation Audio Sounds Autumn In The Forest

Relaxation Audio Sounds Autumn In The Forest

This is an audio all about guiding you to relaxation. This is a Relaxation Audio Sounds with sounds from Autumn In The Forest.

Get My Free MP3 Audio

Post a comment