07.01.1 The Sympathetic Nervous System

They activity of the sympathetic nervous system is controlled by the central nervous system, where the nerves arise, and travel down the spinal cord. The sympathetic nerves come out of the spinal cord at the thoracic-lumbar region, and there are short pre-ganglionic nerves (Figure 7.2). There are two parts of the sympathetic nervous system, one part has ganglia. In the first part, the preganglionic fibres release acetylcholine on to nicotinic receptor on the neurones at the ganglia, and these receptors are known as nicotinic neurone receptors. Activation of the these receptors, leads to the release of noradrenaline from the long post-ganglionic fibres on to an adrenoceptor on an end organ, which is often cardiac or smooth muscle or glands.

Figure 7.2 Sympathetic Nervous System (Copyright QUT, Sheila Doggrell)

In the other part of the sympathetic nervous system, the acetylcholine from the preganglionic fibres is also released on to nicotinic neurone receptors, but these are on specialised ganglia, known as the adrenal medulla. Stimulation of the NN receptors on the adrenal medulla initiates the secretion of adrenaline into the circulation.

As discussed in eChapter 3, there are subdivisions of adrenoceptors. The receptors for noradrenaline and adrenaline were originally called adrenoreceptors but this has been shortened to adrenoceptors over the years. As noradrenaline and adrenaline do not have identical responses in the body, it was decided that there must be more than one kind of adrenoceptors, and the receptors were divided into α- and β-adrenoceptors. Molecular biology techniques have now been able to distinguish 10 subtypes of adrenoceptors. Drugs that stimulate all or most of the adrenoceptor subtypes, which noradrenaline and adrenaline do to a certain extent, will have widespread effects, and these effects can either be beneficial or detrimental. Drugs that select one adrenoceptor will have less widespread effects and, hopefully, less detrimental effects. The effects mediated (functional responses) are well defined for a1-, a2 -, b1-, b2- and b3- adrenoceptors, and we have drugs that can mimic or inhibit these responses. Functional responses are poorly defined for most subdivisions of a1- and a2 -, and b4-adrenoceptors, and we have few drugs that select for these subdivision. The effects mediated by the adrenoceptor subtypes are discussed in the next section.