Big picture
During an examination, the heartbeat can speed up almost immediately, while changes in growth unfold over months. Chemical messengers help coordinate responses operating across these different timescales. Hormones are non-nutrient chemical messengers produced in small amounts and acting on target cells with suitable receptors.
An endocrine gland releases its products into surrounding fluid and blood rather than through a duct. Blood distributes a hormone widely, but receptor distribution determines which cells respond. This explains why a circulating hormone can have specific effects and why normal coordination depends on controlled secretion, transport and receptor function.
Learning goals
Distinguish endocrine, exocrine and mixed glands.
Locate major glands and connect hormones to target functions.
Explain receptor-based action and negative feedback.
Compare blood-glucose and calcium regulation.
Relate hormonal deficiency or excess to characteristic disorders.
Core ideas
1. Chemical signalling and feedback
An endocrine gland is ductless; a sweat gland is exocrine because secretion travels through a duct. The pancreas is mixed: digestive enzymes enter ducts, while islet hormones enter blood. A target cell responds because it possesses a matching receptor, not simply because blood reaches it.
Negative feedback opposes a deviation. When thyroid hormones rise, they inhibit hypothalamic TRH and pituitary TSH, reducing further thyroid stimulation. This is regulation, not a complete permanent shutdown. Hormonal systems interact: stress, nutrition and daily rhythms influence secretion. Avoid interpreting one hormone as controlling every aspect of a physiological process independently.
2. Hypothalamus and pituitary
The hypothalamus links nervous and endocrine coordination. Releasing hormones stimulate anterior pituitary secretion, while inhibiting hormones suppress it; somatostatin inhibits growth-hormone release. The anterior pituitary receives these signals through a specialised portal circulation.
Pituitary region | Hormones | Main actions |
|---|---|---|
Anterior lobe | GH, prolactin, TSH, ACTH, FSH, LH | Growth, milk synthesis and regulation of other endocrine tissues |
Pars intermedia | MSH | Pigment-related action, especially prominent in lower vertebrates |
Posterior lobe | Stores and releases oxytocin and ADH | Uterine contraction, milk ejection and water conservation |
Growth hormone, GH, promotes body growth and metabolism. Deficiency in childhood causes pituitary dwarfism; excess in childhood produces gigantism, while excess after epiphyseal closure produces acromegaly. Prolactin supports milk synthesis. TSH stimulates thyroid secretion; ACTH mainly stimulates adrenal cortex glucocorticoids. FSH and LH regulate gonadal functions.
Oxytocin and antidiuretic hormone, ADH or vasopressin, are synthesised in hypothalamic neurons and released through the posterior pituitary. ADH increases water reabsorption by distal nephron regions. Deficiency can cause diabetes insipidus, characterised by large volumes of dilute urine. Oxytocin promotes uterine contraction and milk ejection, which differs from prolactin's role in making milk.
3. Pineal, thyroid and parathyroids
The pineal gland secretes melatonin, contributing to daily rhythms, sleep–wake timing and seasonal functions. It should not be described as an instant on–off sleep switch. Light-related information affects its rhythmic secretion through neural pathways.
The thyroid gland contains follicles lined by epithelial cells surrounding colloid. It produces the iodine-containing hormones T₃ and T₄, which regulate basal metabolic rate and support normal growth and development. Iodine deficiency can limit synthesis, increasing TSH stimulation and causing goitre. Not every thyroid enlargement has the same cause.
Hypothyroidism in adults lowers metabolic activity. Severe deficiency during fetal and early childhood development can impair brain and physical development. Hyperthyroidism increases metabolic activity; Graves' disease is an autoimmune example often associated with an enlarged thyroid and eye signs. Thyroid parafollicular cells produce calcitonin, which tends to lower blood calcium.
Parathyroid hormone, PTH, is secreted by parathyroid glands and raises blood calcium through effects on bone, kidneys and indirectly intestinal absorption. For example, a fall in blood calcium stimulates PTH rather than a demand for more insulin. Calcium regulation requires balancing multiple tissues, not merely moving calcium into or out of bone in isolation.
4. Thymus and adrenal glands
The thymus, prominent in children and reduced with age, secretes thymosins that support differentiation of T lymphocytes and immune development. Its endocrine role connects coordination with immunity, rather than directly controlling digestion or blood glucose.
Each adrenal gland has an outer cortex and inner medulla with different origins and products. The medulla secretes adrenaline and noradrenaline, catecholamines involved in the fight-or-flight response. Heart rate, breathing and blood availability to active muscles increase; glycogen breakdown helps supply fuel. For example, sudden alarm can produce a rapid coordinated response without requiring new tissue growth.
The cortex produces steroid hormones. Glucocorticoids, chiefly cortisol, influence carbohydrate, protein and fat metabolism and support stress responses. Mineralocorticoids, chiefly aldosterone, promote sodium reabsorption and potassium secretion in kidneys, helping regulate extracellular volume. Small amounts of adrenal androgens also occur. Cortical hyposecretion can cause Addison's disease. Distinguish aldosterone's ion effects from ADH's primary influence on water permeability.
5. Pancreatic islets and glucose balance
The islets of Langerhans contain alpha cells secreting glucagon and beta cells secreting insulin. Insulin lowers blood glucose by promoting cellular uptake in responsive tissues and storage pathways such as glycogenesis. Glucagon raises blood glucose mainly by stimulating hepatic glycogen breakdown and glucose production.
After a carbohydrate-rich meal, increased insulin favours storage; during fasting, glucagon helps maintain a supply to glucose-dependent tissues. These hormones are antagonistic in their effects on blood glucose but do not simply destroy each other chemically. Diabetes mellitus involves persistent hyperglycaemia due to inadequate insulin secretion, impaired action or both. Glucose may appear in urine when renal reabsorptive capacity is exceeded. Diabetes insipidus involves water balance rather than the same glucose-regulation defect.
6. Gonadal hormones
In the testes, Leydig cells secrete androgens, especially testosterone, supporting male reproductive development, secondary sexual characters and reproductive function. Sertoli cells support developing germ cells and secrete inhibin, which contributes negative feedback on FSH.
Ovarian follicles produce oestrogens, supporting female reproductive tissues and secondary sexual characters. After ovulation, the corpus luteum secretes progesterone, helping maintain an endometrium suitable for implantation and supporting pregnancy-related changes. FSH supports follicular growth, while an LH surge triggers ovulation in the normal cycle. In a comparison, identify source, target and function: naming testosterone without Leydig cells or androgen action is incomplete.
7. Hormones from other organs
The heart secretes atrial natriuretic factor, ANF, in response to increased atrial stretch, promoting processes that reduce blood volume and pressure. Kidneys produce erythropoietin, stimulating red blood cell production. Thus an organ need not be exclusively endocrine to release an important hormone.
The digestive tract releases gastrin, secretin, cholecystokinin and gastric inhibitory peptide. Gastrin promotes gastric secretion; secretin stimulates bicarbonate-rich pancreatic secretion; cholecystokinin promotes enzyme secretion and gallbladder contraction. These examples explain how food arriving in one region coordinates secretions elsewhere. Distinguish hormones travelling through blood from digestive enzymes acting directly on food.
8. Mechanisms of hormone action
Water-soluble peptide hormones generally bind membrane receptors because they do not readily cross the lipid bilayer. Receptor activation triggers intracellular signalling, sometimes through second messengers such as cyclic AMP. The response can involve enzyme activity or changes in gene expression. Insulin uses a receptor-associated kinase pathway, so not every membrane hormone acts through cyclic AMP.
Steroid hormones generally enter cells and bind intracellular receptors. Hormone–receptor complexes regulate gene expression and protein synthesis. Thyroid hormones also act largely through intracellular nuclear receptors despite being amino-acid derivatives. For a labelled mechanism diagram, show extracellular messenger, membrane, receptor and intracellular response; for a steroid mechanism, show entry and interaction with gene regulation. Receptor specificity explains why a hormone can circulate everywhere but influence only selected cells.
A reliable approach to questions
Identify the regulated variable: glucose, calcium, water, growth or reproduction.
Name the gland and, where relevant, its region or cell type.
State the hormone's target action before predicting the final physiological change.
Apply feedback to decide whether secretion rises or falls.
Distinguish deficiency from excess and childhood from adult effects.
Connections that matter
Excretion explains ADH and aldosterone effects on nephron water and ion handling.
Reproduction develops gonadotropin, ovarian and testicular feedback loops.
Cell biology explains membrane permeability, receptors and gene regulation.
Common mistakes
Calling the posterior pituitary the synthesis site overlooks hypothalamic production.
Confusing prolactin with oxytocin swaps milk synthesis and milk ejection.
Equating diabetes mellitus with diabetes insipidus confuses glucose and water regulation.
Assigning every membrane hormone to cyclic AMP ignores other signalling pathways.
Revision checklist
I can locate glands and distinguish their regions.
I can connect each major hormone to its source and function.
I can explain negative feedback with a thyroid example.
I can compare insulin with glucagon and ADH with aldosterone.
I can relate receptor location to hormone chemistry.