The autonomic nervous system regulates involuntary actions such as breathing, the regulation of cardiac contractions, blood pressure control, gastrointestinal secretions and motility, control of pupil diameter, sweating, bladder control and sexual function.
The autonomic nervous system is divided into the sympathetic and parasympathetic systems (Figures 21.1 and 21.2). Both systems involve preganglionic and postganglionic fibres. In both cases, acetylcholine (ACh) is the neurotransmitter at the ganglionic synapse, where it stimulates ligand-gated nicotinic receptors, leading to the activation of the postganglionic fibres. These in turn lead to the activation of target receptors on the innervated tissue.
Parasympathetic control
In the parasympathetic nervous system, the ganglion is generally located close to, or in, the innervated organ and generally leads to more localised control. The postganglionic neurotransmitter is Ach, which acts at muscarinic receptors.
Muscarinic receptors are G-protein-coupled receptors (GPCRs) in which the subtypes M1, M3 and M5 are coupled via Gq/11 to Ca2+ mobilisation; and M2 and M4 are Gi-linked to inhibition of formation of the second messenger cAMP (Chapter 7).
Sympathetic control
Anatomically this tends to provide more ‘global’ control, with the autonomic ganglia or synapses being located more centrally and closer to the spinal cord. The postganglionic neurotransmitter is noradrenaline (Figure 21.3), which acts at α- or β-adrenoceptors, depending on the tissue. An exception are the sweat glands, which are functionally sympathetic but have ACh as the neurotransmitter, which stimulates muscarinic (M) receptors.
An extension of the sympathetic nervous system is the adrenal medulla, which is essentially a sympathetic postganglionic fibre where ACh acts at nicotinic receptors to stimulate the release of adrenaline (and some noradrenaline) into the circulation. Adrenaline then exerts sympathetic actions (e.g. increase in heart rate and bronchodilation). This forms part of the ‘fright, flight or fight’ response.
Adrenoceptors
α1-adrenoceptors are coupled via G-proteins (Gq/11) to activation of phospholipase C, which liberates inositol trisphophate (IP3) and diacyl glycerol (DAG), leading to increases in intracellular Ca2+.
α2-adrenoceptors are negatively coupled via Gi to adenylyl cyclase, leading to reductions in cAMP.
β1– and β2-adrenoceptors are also GPCRs in which Gs is coupled to the activation of adenylyl cyclase and elevations in cAMP.
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