The adrenal glands

The two adrenal glands sit like cocked hats over each kidney (Fig. 5.9) (hence their name - additions to the renal organ, or kidney). Each gland has an inner core and an outer layer of cells, the adrenal medulla and adrenal cortex respectively. The cortex (outer layer) makes up about nine-tenths of the bulk of the gland; its cells under the microscope are rich in lipid. The medulla stains darkly for microscopy with chromic salts, showing the presence of so-called chromaffin cells, characterised by the presence of catecholamines (such as adrenaline and noradrenaline).

Left adrenal Diaphragm (cut) Right adrenal

Left adrenal Diaphragm (cut) Right adrenal

Abdominal blood vessels

Fig. 5.9 The anatomy of the adrenal glands.

Abdominal blood vessels

Fig. 5.9 The anatomy of the adrenal glands.

5.5.1 The adrenal cortex: Cortisol secretion

The adrenal cortex secretes a number of steroid hormones which are synthe-sised from cholesterol. Some of these affect mainly mineral metabolism (salt and water balance) and are known collectively as the mineralocorticoids; some affect intermediary metabolism (glucose, fatty acid and amino acid metabolism) and are known as the glucocorticoids. The most important of these in humans is cortisol.1

As we have seen, the synthesis and secretion of cortisol are regulated by ACTH from the anterior pituitary. Cortisol has metabolic effects on a number of tissues. They are both short-term and longer-term. Even the short-term effects are for the most part mediated by changes in protein synthesis and therefore take a matter of hours rather than minutes. These include: a stimulation of fat mobilisation in adipose tissue, by increased activity of the enzyme hormonesensitive lipase (this probably involves synthesis of additional enzyme protein); a stimulation of gluconeogenesis (again via synthesis of key enzymes; see Box 4.2); inhibition of the uptake of glucose by muscle (mechanism not clear); and an increase in the breakdown of muscle protein (see Section 6.3.3).

These effects of cortisol are often difficult to demonstrate in isolated tissues, and it is thought that many of cortisol's effects are more permissive than direct. A permissive effect means that a process cannot occur (or activation by another hormone cannot occur) in the absence of the 'permitting agent' - in this case cortisol - but the actual level of the permitting agent is not important. Thus, in people or animals whose adrenal cortex has been removed, some effects of adrenaline, for instance, do not occur (particularly stimulation of glycogen breakdown). Responsiveness to adrenaline can be reinstated by giving a glucocorticoid hormone such as cortisol, but the level achieved is not important

- just its presence. This is certainly an oversimplification for most of cortisol's effects, but it is probably true that cortisol 'sets the tone' of response to other hormones.

5.5.2 The adrenal medulla, adrenaline secretion and adrenaline action

The adrenal medulla develops as part of the nervous system. It is supplied with nerves that are part of the sympathetic nervous system. (They are pregangli-onic fibres whose neurotransmitter is acetylcholine; this will be discussed in detail in Section 7.2.2.1.) Its secretory activity is controlled directly by the brain through these nerves, and not by substances in the blood. It secretes the hormone adrenaline (named, of course, after the adrenal gland; in American literature this hormone is called epinephrine). More will be said about adrenaline and the related compound noradrenaline (norepinephrine in American) in a later chapter (Section 7.2.3.1); for now, it is satisfactory to think of them as having similar effects, although noradrenaline is almost entirely liberated as a neurotransmitter from sympathetic nerve terminals, and is therefore not a true hormone, whereas adrenaline is a hormone in every sense. They are both referred to as catecholamines because they are amine derivatives of the catechol nucleus. Their structures and the route of synthesis are shown in Fig. 5.10.

Adrenaline and noradrenaline act on adrenergic receptors (or adrenoceptors), found in the plasma membranes of most tissues. The adrenoceptors are 7-transmembrane domain (or serpentine) G-protein coupled receptors (see Box 2.3). There are different types of adrenergic receptor, first recognised because of the different potencies of adrenaline-like substances in bringing about various effects in specific tissues. Broadly, they may be divided into the a- and P-receptors, which are themselves subdivided into ax, a2, and P13 subtypes; the P3 subtype is probably confined in humans to brown adipose tissue. The subtypes of adrenergic receptors are summarised in Table 5.1.

Binding of adrenaline and noradrenaline to adrenergic receptors brings about a variety of effects. From the point of view of energy metabolism, we will divide these into two groups: circulatory effects, and direct metabolic effects. The two are not independent, as will become clear in later sections.

P-Adrenergic receptors are linked, via the stimulatory Gs proteins, to the membrane-bound enzyme adenylyl cyclase which produces cyclic adenosine 3' ,5' -monophosphate (cAMP) from ATP (see Box 2.3). Binding of adrenaline or noradrenaline to a P-adrenergic receptor thus causes an increase in cytosolic cAMP concentration, and activation of the cAMP-dependent protein kinase (also known as protein kinase-A; see Box 2.3). This may lead (directly or through other protein kinases) to phosphorylation of a key regulatory enzyme: glycogen phosphorylase and hormone-sensitive lipase are two examples (see Box 2.4). Thus, catecholamines acting through P-adrenergic receptors tend to lead to breakdown of stored fuels, triacylglycerol and glycogen. The circulatory effects of P-adrenergic receptors are mainly stimulatory, especially

DOPA decarboxylase
Fig. 5.10 Biosynthesis of the catecholamines. Noradrenaline is released from sympathetic nerve terminals, whereas adrenaline is a true hormone, released into the bloodstream from the adrenal medulla.
Table 5.1 Adrenergic receptors and their effects.

Receptor type

How To Boost Your Metabolism

How To Boost Your Metabolism

In The Next 45 Minutes You're Going To Discover How To Boost Your Metabolism And Lose Weight. Who Else Wants To Boost Their Metabolism And Shed Pounds Fast?

Get My Free Ebook


Post a comment