Sympathetic Nervous System

The cell bodies of the sympathetic preganglionic fibres are in the lateral horns of the spinal segments T1-L2, the so called thoraco-lumbar outflow. The preganglionic fibres travel a short distance in the mixed spinal nerve, and then branch off as white rami (myelinated) to enter the sympathetic ganglia. These are mainly arranged in two paravertebral chains which lie anterolateral to the vertebral bodies and extend from the cervical to the sacral region. They are called the sympathetic ganglionic chains. The short preganglionic fibres which enter the chain make a synapse with a postsynaptic fibre either at the same dermatomal level, or at a higher or lower level, and then the longer postganglionic fibres usually return to the adjacent spinal nerve via grey rami (unmyelinated) and are conveyed to the effector organ.

Some preganglianic fibres do not synapse in the sympathetic chains but terminate in separate cervical or abdominal ganglia, or travel in the greater splanchnic nerve and directly synapse with chromaffin cells in the adrenal medulla. As discussed above, Ach is the neurotransmitter via a nicotinic receptor at the preganglionic synapse. The adrenal medulla is innervated by preganglionic fibres and therefore adrenaline is released from the gland by stimulation of nicotinic Ach receptors.

At most postganglionic sympathetic endings, the chemical transmitter is noradrenaline, which is present in the presynaptic terminal as well as in the adrenal medulla. In sweat glands, however, postganglionic sympathetic fibres release Ach and this transmission is nicotinic.

Adrenaline and noradrenaline are both cate-cholamines, and are both synthesized from the essential amino acid phenylalanine by a series of steps, which includes the production of dopamine. The terminal branches of the sympathetic postganglionic fibres have varicosities or swellings, giving them the appearance of a string of beads. These swellings form the synaptic contact with the effector organ, and are also the site of synthesis and storage of noradrenaline. On the arrival of a nerve impulse, noradrenaline is released from granules in the presynaptic terminal into the synaptic cleft. The action of noradrenaline is terminated by diffusion from the site of action, re-uptake back into the presynaptic nerve ending where it is inactivated by the enzyme Monoamine Oxidase in mitochondria or metabolism locally by the enzyme Catechol-O-Methyl-Transferase.

The synthesis and storage of catecholamines in the adrenal medulla is similar to that of sympathetic postganglionic nerve endings, but due to the presence of an additional enzyme the majority of noradrenaline is converted to adrenaline. The adrenal medulla responds to nervous impulses in the sympathetic cholinergic preganglionic fibres by transforming the neural impulses into hormonal secretion. In situations involving physical or psychological stress, much larger quantities are released.

The actions of catecholamines are mediated by specific postsynaptic cell surface receptors. Pharmacological subdivision of these receptors into two groups (alpha and beta) was first suggested by Ahlquist in 1948, based upon the effects of adrenaline at peripheral sympathetic sites. These have since been further subdivided on functional and anatomical grounds. Thus beta₁-adrenoceptor mediated effects in the heart (increased force and rate of contraction) have been differentiated from those producing smooth muscle relaxation in the bronchi and blood vessels (beta₂ effects). Similarly, alpha-adrenoceptor mediated effects such as vasoconstriction have been termed, alpha₁- effects, to differentiate them from the feedback inhibition by noradrenaline on its own release from presynaptic terminals, which is mediated by alpha₂-adrenoceptors on the presynaptic membrane.

However, further research now shows that the classification is not as simple as this. For instance, many organs have both beta₁ and beta₂ adrenoceptors. (e.g. in the heart, there is one beta₂-adrenoceptor to every three beta₁-adrenoceptors). The receptors also show differing responses to adrenaline and noradrenaline. At beta₁ adrenoceptors in the heart, adrenaline and noradrenaline appear to have an equal effect, whereas at beta₂ adrenoceptors in smooth muscle are more sensitive to circulating adrenaline than noradrenaline.

This article contained links to the following additional information:

Table 1: Responses of major organs to autonomic nerve impulses

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