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Adrenal Glands - Basic Adrenal Physiology

In This Article

 

Introduction

This article explains the production and effects of adrenal products. For more information on mechanisms of blood pressure regulation, secretion of ions, and other effects related to the action of mineralocorticoids, please see this article.

  • The adrenal glands are also sometimes known as suprarenal glands
  • They sit on top of the kidneys. They weight about 4g, and have a medulla and a cortex, like the kidneys themselves.
  • The medulla – is directly connected to the sympathetic nervous system, and will secrete adrenaline and noradrenaline in response to sympathetic stimulation.
  • These two hormones cause almost the exact same effects on body tissues as direct sympathetic stimulation itself does.
  • The cortex secretes an entirely different type of hormone – corticosteroids. The corticosteroids are all synthesised from cholesterol, and have similar chemical formulas.
  • There are three types of corticosteroid:
    • Mineralcorticoids – e.g. aldosterone - these are so called because they effect the ‘minerals’ (electrolytes) of the blood. They particularly effect sodium and potassium.
    • Glucocorticoids – e.g. cortisol - so called due to their effects on glucose metabolism – however they also have important effects on protein and fat metabolism.
    • Androgens – these are sex hormones that exhibit similar effects to testosterone. They are not particularly important, except in disease of the adrenal glands where their hypersecretion can result in masculization.
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Anatomy

  • The zona glomerulosa – this constitutes about 25% of the adrenal cortex, and it is where aldosterone is produced – this region contains the enzyme aldosterone synthase. The production of aldosterone is controlled by extracellular fluid concentrations of angiotensin II and potassium. Both these two chemicals will increase the synthesis of aldosterone. Prolonged stimulation of this zone can lead to its hypertrophy.
  • The zona fasciculata - this constitutes about 75% of the adrenal cortex, and secretes glucocorticoids as well as small amounts of androgens and oestrogens. The secretion of these hormones is largely controlled by the hypothalamic-pituitary axis – and the release of ACTH (adrenocorticotropic hormone).
  • The zona reticularis – this is responsilbe for most of the androgen output of the adrenal galnd and it also secretes some oestrogens and glucocorticoids.
  • The mechanisms of androgen secretion are not well understood in comparison with the mechanisms of mineralcorticoid and glucocorticoid secretion.
 
 
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Corticosteroids

The term ‘corticosteroid’ can actually refer to both mineralocorticoids (i.e. aldosterone) and to glucocorticoids, i.e. to the hormones produced in the adrenal cortex.
Often a ‘mineralocorticoid’ will also have some glucocorticoid activity, and vice-versa.
 
All corticosteroids are synthesised from cholesterol. The adrenal cortex is capable of synthesising its own cholesterol from acetate, however, >80% of the cholesterol it uses comes from LDL’s circulating in the blood. LDL’s have high concentrations of cholesterol and are absorbed from coated pits by endocytosis into adrenal cells.
  • ACTH will cause an increase in corticosteroid synthesis by both increasing the number of surface receptors for LDL’s and it will also increase the number of enzymes used to liberate cholesterol from endocytosed LDL’s.
  • Note that stress also causes an increase in cortisol production.
  • The rate limiting step in to production of adrenal hormones is the first step in cholesterol breakdown, which occurs in the mitochondria by the enzyme cholesterol desmolase.
  • ACTH and angiotensin II will both increase the rate of this reaction.
  • There are then a series of reactions in the mitochondria, and then later on the ER that lead to the production of hormones. Obviously, some of these reactions differ depending on which region of the cortex you are in.
Corticosteroids are transported in the blood bound to plasma proteins. Aldosterone tends to bind to albumin. About 40% of aldosterone remains free, giving it a half-life of about 20 minutes. Cortisol ion the other hand binds to cortisol binding globulin (aka transcortin) as well as to albumin. This means there is much less free cortisol in the blood and as a result, cortisol has a half-life of 60-90 minutes.
The general effect of these binding globulins is that it helps buffer sudden changes in concentration of the corticosteroids, such as in brief periods of stress, or when ACTH is released. Binding proteins also ensure that there is a uniform distribution of corticosteroids to the peripheral tissues.
Corticosteroids are metabolised by the liver. They are converted mainly into glucuronic acid and to a lesser extent sulphates. These metabolites are inactive and have no glucocorticoid or mineralocorticoid activity. 25% of the metabolites are removed by the liver, whilst the rest enter general circulation and remain unbound in plasma, and they are then removed by the kidneys.
Diseases of the liver directly reduce the excretion of these products.
 
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Mineralocorticoids 

e.g. aldosterone, cortisol, cortisone
Many mineralocorticoids also have glucocorticoid activity!
Aldosterone is responsible for over 90% of the activity of mineralocorticoids. Cortisol is only responsible for a very small amount of activity, but it is secreted in very large amounts (it is responsible for a LOT of glucocorticoid activity!)
Cortisone is a synthetic corticoid, with lots of glucocorticoid activity, but not much mineralocorticoid activity. Generally, the synthetic glucocorticoids (e.g. cortisone and dexamethasone) have no or very little mineralocorticoid activity.
Cortisol is particularly relevant in pathological instances – it has relatively little mineralocorticoid activity, but in excess this can become noticeable – however it will also cause significant glucocorticoid issues!
Without mineralocorticoids, potassium concentration in the extracellular fluid rises rapidly, sodium and chloride are rapidly lost from the body, as is a lot of fluid. The individual will develop diminished cardiac output, and will enter a shock like state, before death occurs, if no treatment is administered.
 
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