Effects of the autonomic nervous system on hormone secretion

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The pancreatic islets have both a- and P-adrenergic receptors, and are innervated by sympathetic nerves. They also receive fibres of the parasympathetic nervous system. These nerves regulate the secretion of both insulin and glu-cagon, as summarised in Table 7.2. These influences on pancreatic hormone secretion probably operate at the level of 'fine tuning' in normal daily life, and it is not easy to demonstrate their role. In rodents, there is undoubtedly a normal adrenergic restraint on insulin secretion, since the plasma insulin concentration rises if the adrenal medullas are removed. In humans, the effects of adrenergic blocking drugs in the whole body are very difficult to interpret because they cause such widespread changes in both circulation and metabolism. The effects of the parasympathetic innervation of the pancreatic islets are undoubtedly

Table 7.2 Adrenergic and parasympathetic effects on hormone secretion from the pancreas.


Insulin secretion

Glucagon secretion


Suppresses (dominant effect)



Increases (only seen if a-effects blocked)





Sources: Robertson & Porte (1973); Bloom et al. (1974); Humphrey et al. (1975a, b); Brunicardi et al. (1987).

Sources: Robertson & Porte (1973); Bloom et al. (1974); Humphrey et al. (1975a, b); Brunicardi et al. (1987).

important. They mediate the 'cephalic phase' of insulin secretion in response to the sight or smell of food, mentioned in Chapter 3 (Section 3.2.1). Also, in patients whose vagus nerve is cut at surgery to reduce gastric acid secretion (a former treatment for gastric ulcers), insulin secretion in response to a glucose drink is impaired, as is glucagon secretion in response to hypoglycaemia.

However, the effects of the nervous system (particularly adrenergic influences) on pancreatic hormone secretion become of great importance in 'stress' situations such as strenuous exercise or physical injury. In these situations, there is P-adrenergically mediated stimulation of glucagon secretion, and a-adrenergic suppression of insulin secretion. These mechanisms reinforce the mobilisation of fuel stores (glycogen and triacylglycerol) and, in the case of physical injury, reinforce the resultant hyperglycaemia (elevation of the blood glucose concentration). During strenuous exercise, glucose utilisation by exercising muscle is increased greatly by insulin-independent mechanisms, so these effects may be seen as a means of maximising the availability of energy-providing substrates to the muscles without compromising glucose utilisation. (Metabolism during exercise will be covered in Chapter 8.)

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