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- Hormonal Communication
Hormonal Communication¶
Part of Module 5: Communication, homeostasis and energy.
The endocrine system provides a chemical communication network that complements the nervous system. Where neuronal signals are fast, targeted and brief, hormonal signals are slower, widespread and sustained. This makes hormones ideal for regulating metabolic processes that need continuous fine-tuning — blood glucose, water balance, growth and the stress response. The pancreas and adrenal glands are the key examples in this topic.
Learning Objectives¶
| ID | Official specification wording | Main teaching sections |
|---|---|---|
5.1.4-lo-1 |
(a) endocrine communication by hormones | Hormones and Endocrine Glands |
5.1.4-lo-2 |
(b) the structure and functions of the adrenal glands (c) (i) the histology of the pancreas (ii) the examination and drawing of stained sections of the pancreas to show the histology of the endocrine tissues |
The Adrenal Glands, The Fight or Flight Response |
5.1.4-lo-3 |
(d) how blood glucose concentration is regulated | The Pancreas and Blood Glucose Regulation |
5.1.4-lo-4 |
(e) the differences between Type 1 and Type 2 diabetes mellitus (f) the potential treatments for diabetes mellitus. |
Second Messenger Model, Diabetes Mellitus, Nervous Control of Heart Rate |
Hormones and Endocrine Glands¶
A hormone is a chemical messenger secreted directly into the blood by a ductless endocrine gland. It is carried in the blood to all tissues, but only cells possessing specific complementary receptors on their plasma membrane (or, for steroid hormones, inside the cell) can respond. These cells are called target cells.
The sequence of events for any hormone is: 1. Endocrine gland cells produce the hormone 2. When stimulated, the gland releases the hormone into the bloodstream 3. Blood carries the hormone to target cells throughout the body 4. The hormone attaches to receptors on or inside the target cells 5. Target cells respond to produce a physiological effect
Comparing Hormonal and Neuronal Communication¶
| Feature | Neuronal communication | Hormonal communication |
|---|---|---|
| Signals | Nerve impulses | Hormones |
| Transmission | Along neurones | By blood |
| Speed | Very fast (milliseconds) | Slower (seconds to minutes) |
| Range | Specific, localised | Body-wide, widespread |
| Duration of effect | Brief, ends when impulse stops | Prolonged |
| Examples | Reflex arcs, voluntary movement | Insulin, adrenaline, ADH |
Types of Hormone¶
Hormones fall into two classes with very different mechanisms of action:
| Feature | Non-steroid (peptide) hormones | Steroid hormones |
|---|---|---|
| Solubility | Water soluble (hydrophilic) | Lipid soluble (hydrophobic) |
| Can diffuse across phospholipid bilayer? | No | Yes |
| Mechanism of action | Bind to receptors on cell-surface membrane; activate second messengers inside the cell | Diffuse through the membrane; bind to receptor molecules in cytoplasm or nucleus, forming a hormone-receptor complex that acts as a transcription factor |
| Example | Adrenaline, insulin, glucagon | Oestrogen, cortisol, aldosterone |
Endocrine glands are ductless — they secrete hormones directly into the blood. By contrast, exocrine glands secrete their products through a duct to a target organ. The pancreas is unusual in being both: - Endocrine: Islets of Langerhans secrete insulin and glucagon into the blood - Exocrine: Acinar cells (pancreatic acini) secrete digestive enzymes (amylases, proteases, lipases) and alkaline pancreatic juice through the pancreatic duct into the duodenum
The Adrenal Glands¶
The adrenal glands are a pair of small, triangular endocrine glands located above each kidney. Each gland consists of two structurally and functionally distinct regions surrounded by a capsule:
- Adrenal cortex — the outer region, produces steroid hormones
- Adrenal medulla — the inner region, produces catecholamine hormones
Adrenal Cortex¶
The adrenal cortex synthesises and releases three groups of steroid hormones, each with specific functions. Their release is regulated by chemical signals from the hypothalamus and kidneys:
| Hormone group | Functions | Examples |
|---|---|---|
| Glucocorticoids | Regulate metabolism (conversion of fats, proteins and carbohydrates to energy); control blood pressure and stress responses; regulate the immune response and suppress inflammation | Cortisol, corticosterone |
| Mineralocorticoids | Maintain blood pressure by balancing salt and water in blood and body fluids; stimulate reabsorption of Na⁺ (and consequently water) in the distal convoluted tubule in exchange for K⁺ | Aldosterone |
| Androgens | Regulation of sexual characteristics and cell growth | Testosterone |
Cortisol stimulates gluconeogenesis (synthesis of glucose from non-carbohydrate sources) and promotes breakdown of proteins and lipids to maintain blood glucose during stress.
Aldosterone targets the distal convoluted tubule and collecting duct of the nephron, regulating blood pressure and ion balance.
Adrenal Medulla¶
The adrenal medulla produces catecholamines — hormones that prepare the body for stressful or dangerous situations. They are released when the sympathetic nervous system is stimulated.
Adrenaline effects: - Increases heart rate and blood pressure to increase blood flow to muscles and brain - Increases blood glucose levels - Increases breathing rate - Dilates bronchioles
Noradrenaline effects: - Increases heart rate - Expands air passages - Dilates pupils - Narrows blood vessels in organs like the gut (reducing blood flow to regions unhelpful in the stress response)
The Fight or Flight Response¶
The fight or flight response is an instinctive reaction to perceived threats involving complex coordination between the nervous and endocrine systems.
Mechanism¶
- The autonomic nervous system detects a threat; the signal is passed to the hypothalamus
- The hypothalamus activates the sympathetic nervous system, sending nerve signals to glands and muscles
- The sympathetic nervous system triggers secretion of adrenaline and noradrenaline from the adrenal medulla
- The hypothalamus also communicates with the adrenal-cortical system, stimulating the pituitary gland to release ACTH (adrenocorticotropic hormone)
- ACTH travels via the bloodstream to the adrenal cortex, stimulating release of glucocorticoids and other hormones to help the body deal with the threat
Physiological Responses¶
| Physiological reaction | Purpose |
|---|---|
| Increased heart rate | Circulate more oxygenated blood to muscles |
| Pupil dilation | Improve vision |
| Constriction of arterioles in skin | Divert blood to major muscles, brain, and heart |
| Rise in blood glucose levels | Increase cellular respiration |
| Relaxation of airway muscles | Allow more oxygen into the lungs |
| Digestion stops | Prioritise emergency bodily functions |
The Pancreas and Blood Glucose Regulation¶
The Islets of Langerhans¶
The pancreas is predominantly exocrine tissue, but scattered throughout are approximately one million clusters of endocrine cells called the Islets of Langerhans. They contain two main cell types:
| Cell type | Hormone secreted | Response to blood glucose |
|---|---|---|
| Alpha (α) cells | Glucagon | Released when blood glucose is too low |
| Beta (β) cells | Insulin | Released when blood glucose is too high |
Both cell types are specialised for efficient hormone production and secretion: - Many ribosomes and rough ER for protein synthesis (both hormones are polypeptides) - Well-developed Golgi apparatus for packaging hormones into secretory vesicles - Many mitochondria providing ATP for active cellular processes - Hormones are released by exocytosis of secretory vesicles
Why Blood Glucose Must Be Regulated¶
The normal blood glucose concentration is approximately 90 mg per 100 cm³ (~5 mmol L⁻¹). Regulation is critical because: - Glucose is the primary respiratory substrate for most cells, and the only substrate for brain cells under normal conditions - Hyperglycaemia (too high) causes osmotic problems (drawing water from cells), and glucose may appear in urine (glycosuria), representing wasted energy - Hypoglycaemia (too low) deprives cells — especially neurones — of their energy source, causing confusion, loss of consciousness and eventually death
Response to High Blood Glucose (After a Meal)¶
- Rise in blood glucose is detected directly by β cells
- β cells secrete insulin into the blood; insulin secretion inhibits α cells from releasing glucagon
- Insulin binds to insulin receptors on target cells (liver hepatocytes, adipose cells, muscle cells)
- Binding causes vesicles containing GLUT4 glucose transporter proteins to fuse with the cell membrane, increasing membrane permeability to glucose
- Glucose uptake into cells increases; increased respiration breaks down more glucose
- In hepatocytes and muscle cells: glucose → glycogen (glycogenesis)
- In adipose tissue: glucose → fatty acids and triglycerides (lipogenesis)
Result: Blood glucose concentration falls back towards the set point.
Response to Low Blood Glucose (During Fasting or Exercise)¶
- Fall in blood glucose detected by α cells
- α cells secrete glucagon; glucagon secretion inhibits β cells from releasing insulin; reduced respiration decreases glucose breakdown
- Glucagon binds to receptors on hepatocytes
- Hepatocytes break down glycogen → glucose (glycogenolysis)
- In prolonged fasting: hepatocytes synthesise glucose from amino acids and glycerol (gluconeogenesis)
- Glucose diffuses out of hepatocytes into the blood
Result: Blood glucose concentration rises back towards the set point.
Adrenaline also works with glucagon to increase blood glucose when levels are too low, by promoting glycogenolysis and gluconeogenesis in liver and muscle cells.
The insulin/glucagon system is a classic negative feedback loop (see 5.1.1 Communication and homeostasis): the correction mechanism opposes the original deviation.
Mechanism of Insulin Secretion from β Cells¶
The β cell is itself a glucose sensor. The mechanism is known as stimulus-secretion coupling:
- Blood glucose rises → glucose diffuses into β cells through GLUT2 transporters (down concentration gradient)
- Glucose undergoes glycolysis and further respiration, generating ATP
- Rising ATP concentrations cause ATP-gated K⁺ channels to close
- K⁺ can no longer leave; the inside of the cell becomes less negative → depolarisation
- Depolarisation opens voltage-gated Ca²⁺ channels; Ca²⁺ enters the cell
- Ca²⁺ influx stimulates exocytosis of insulin-containing secretory vesicles
- Insulin is released into surrounding capillaries
This mechanism couples insulin secretion directly to cellular energy metabolism, ensuring insulin is only released when glucose is genuinely available.
Second Messenger Model¶
Non-steroid hormones cannot cross the plasma membrane because they are water-soluble. Instead they use a second messenger system. Adrenaline provides the clearest example of this pathway:
- Adrenaline (first messenger) binds to a complementary adrenergic receptor on the cell-surface membrane of a liver cell
- Binding causes the receptor protein to change shape, activating a G protein
- The G protein activates the enzyme adenylyl cyclase (adenylate cyclase)
- Adenylyl cyclase converts ATP → cyclic AMP (cAMP) inside the cell
- cAMP (second messenger) activates many protein kinases via phosphorylation — the signal is amplified at each stage (the cascade effect)
- Protein kinases activate enzymes that catalyse glycogenolysis (breakdown of glycogen → glucose) in liver cells
- Glucose moves out of liver cells by facilitated diffusion and enters the blood
- Blood glucose concentration rises, providing more glucose for respiration in body cells
Amplification: one hormone molecule generates multiple cAMP molecules, each activating multiple protein kinases, each activating multiple downstream enzymes. This means even small concentrations of hormone can produce a large cellular response.
Termination: cAMP is rapidly broken down by phosphodiesterase to terminate the signal.
Diabetes Mellitus¶
Diabetes mellitus is a condition characterised by improperly regulated blood glucose levels. One sign of diabetes is glucose in urine, indicating blood glucose levels exceed the renal threshold (kidneys cannot reabsorb all filtered glucose).
Type 1 vs Type 2 Diabetes¶
| Feature | Type 1 diabetes | Type 2 diabetes |
|---|---|---|
| Underlying cause | Autoimmune destruction of β cells | Cells develop insulin resistance; β cell function may also decline |
| Insulin production | Very little or none | Initially normal or raised; later may decline |
| Onset | Typically childhood/early adulthood | Typically later in life; increasingly in younger people |
| Risk factors | Genetic; possibly triggered by viral infection | Obesity, high-sugar diet, sedentary lifestyle, ethnicity, age |
| Treatment | Insulin injections or pump; blood glucose monitoring; pancreatic islet transplant | Diet, exercise, oral medication; insulin injections if needed |
Symptoms of Uncontrolled Diabetes¶
- Glycosuria (glucose in urine) — blood glucose exceeds renal threshold
- Polyuria (frequent urination) — osmotic diuresis caused by glucose in filtrate
- Polydipsia (excessive thirst) — fluid loss drives thirst
- Fatigue — cells cannot access glucose effectively
- Ketoacidosis (Type 1) — in the absence of insulin, fat is broken down rapidly; ketone bodies accumulate, lowering blood pH
Modern Insulin Production¶
People with Type 1 diabetes require exogenous insulin. Genetically engineered bacteria (e.g. E. coli) carrying the human insulin gene inserted into a plasmid vector now produce human insulin for medical use. Advantages: - Identical amino acid sequence to human insulin → lower risk of immune reaction - Can be produced in large quantities - No ethical or religious objections (unlike animal-derived insulin) - Lower production costs
Potential Future Treatments¶
Stem cell therapy: stem cells have the ability to develop into any cell type. Research is exploring growing stem cells into β cells and implanting them into the pancreas of people with Type 1 diabetes, enabling their own insulin production. This treatment remains in the research phase but holds significant potential.
Nervous Control of Heart Rate¶
The sinoatrial node (SAN) sets the heart's basic rhythm. The brain and autonomic nervous system can modify the heart rate according to the body's demands.
The medulla oblongata acts as the control centre. It receives information from two types of receptor in the carotid arteries and aorta:
- Baroreceptors — detect blood pressure
- Chemoreceptors — detect blood chemistry (O₂, CO₂, pH)
The medulla oblongata then adjusts the SAN's firing rate via the autonomic nervous system:
| Stimulus | Receptors | Autonomic pathway | Neurotransmitter | Effect on SAN | Change in heart rate |
|---|---|---|---|---|---|
| High blood pressure | Baroreceptors | Parasympathetic | Acetylcholine | Decreased electrical activity | Decreases |
| Low blood pressure | Baroreceptors | Sympathetic | Noradrenaline | Increased electrical activity | Increases |
| High O₂, low CO₂, or high pH | Chemoreceptors | Parasympathetic | Acetylcholine | Decreased electrical activity | Decreases |
| Low O₂, high CO₂, or low pH | Chemoreceptors | Sympathetic | Noradrenaline | Increased electrical activity | Increases |
Example: Heart Rate Control During Exercise¶
During exercise, blood CO₂ concentration rises and pH falls: 1. Chemoreceptors in the carotid arteries and aorta detect the change and increase impulse frequency to the medulla oblongata 2. The medulla increases impulses to the SAN via the sympathetic nervous system 3. Heart rate increases, delivering more O₂ to active muscles and removing excess CO₂ via the lungs 4. As exercise slows, CO₂ falls and pH rises; the parasympathetic pathway slows the heart back towards resting rate
Hormones such as adrenaline and noradrenaline also influence heart rate directly — in times of stress, they cause the SAN to increase the heart rate as part of the fight or flight response.
Key Terms¶
- Hormone: a chemical messenger released by endocrine cells and carried in the blood to target cells.
- Endocrine gland: a gland that secretes hormones directly into the bloodstream.
- Target cell: a cell that carries the complementary receptor for a particular hormone.
- Adrenaline: hormone released by the adrenal medulla that prepares the body for fight or flight.
- Insulin: hormone from pancreatic beta cells that lowers blood glucose concentration.
- Glucagon: hormone from pancreatic alpha cells that raises blood glucose concentration.
- Glycogenesis: conversion of glucose to glycogen for storage.
- Glycogenolysis: breakdown of glycogen to glucose.
- Gluconeogenesis: synthesis of glucose from non-carbohydrate precursors (amino acids, glycerol) in the liver.
- Second messenger: intracellular signalling molecule generated after a hormone binds at the cell surface.
- cAMP: cyclic AMP, a common second messenger that activates enzyme cascades inside cells.
- Stimulus-secretion coupling: the mechanism in β cells by which a rise in blood glucose triggers insulin release via ATP-mediated closure of K⁺ channels and Ca²⁺ influx.
- Baroreceptor: stretch-sensitive receptor that detects changes in blood pressure.
- Chemoreceptor: receptor that detects chemical changes such as CO2 concentration or pH.