Integrated Systems Anatomy & Physiology – Control of Body Systems (Module 1, Lecture Part 3) Study Notes

Module: Control of Body Systems – Integrated Systems Anatomy & Physiology
Part 3 of 4 in the lecture sequence delivered by Dr Gary Whittaker (School of Pharmacy & Biomedical Sciences, Curtin University)
Builds directly on:
- Fundamental physiology learned in HSF100
- Selected readings from Seeley’s Anatomy & Physiology (12ᵗʰ ed.), Ch. 12, 13, 14, 17, 18 (focus pages 579–598)

Autocrine
- Chemical signal acts on the same cell that secreted it
- Example: White-blood-cell (WBC) cytokines that self-regulate immune activity
Paracrine
- Signal diffuses to nearby cells (localised action)
- Example: WBC-derived histamine → local vasodilation/inflammation
Endocrine
- Chemical (hormone) enters bloodstream → acts on distant target cells/tissues possessing the specific receptor
- Distinguished from neurotransmitters, which act across a synapse

Endocrine glands
- Ductless; secrete hormones into interstitial fluid → diffuse into capillaries → circulate in blood
- Examples: pituitary, thyroid, ovaries, testes
Exocrine glands
- Possess ducts; release non-hormonal secretions to a body surface or lumen
- Examples: sweat, salivary, lacrimal, mucous glands

Amino-acid based (water-soluble)
- Single amino acids, peptides, or full proteins
- Example pool: ALL pituitary hormones (ACTH, LH, FSH, TSH, ADH, etc.)
- Exception: Thyroid hormones T₃ (triiodothyronine) & T₄ (tetraiodothyronine) are derived from tyrosine but behave like steroids (lipid-soluble)
Steroid or lipid-derived (lipid-soluble)
- Synthesised from cholesterol or fatty acids
- Examples: testosterone, progesterone, oestrogen, aldosterone, cortisol

Dictates blood-transport strategy (free vs bound)
Determines cell-receptor location (membrane vs intracellular)
Controls whether action is direct (gene modulation) or indirect (second-messenger cascade)

Water-soluble hormones
- Dissolve directly in plasma → circulate as free hormones
- Are rapidly degraded; short half-life → require continuous secretion for prolonged effect
Lipid-soluble hormones
- Cannot dissolve in aqueous plasma; bind reversibly to specific carrier proteins
- Binding keeps hormone within vasculature; at tissues, hormone dissociates → diffuses into cells

Target-cell response requires presence of specific receptor
- Intracellular receptors (cytoplasm or nucleus) ↔ lipid-soluble hormones that can cross the phospholipid bilayer
- Membrane-bound receptors ↔ water-soluble hormones that cannot permeate the membrane

Steps
1. Hormone diffuses through lipid bilayer
2. Binds intracellular receptor → forms hormone–receptor complex
3. Complex enters nucleus via nuclear envelope pores
4. Binds DNA at specific hormone-response elements → initiates or inhibits transcription
5. mRNA → ribosomes → altered protein synthesis (structural & enzymatic proteins)
Results
- Long-term changes: organelle proliferation, metabolic shifts, developmental effects
Applicable hormones: corticosteroids, sex steroids, T3 & T4

Second-messenger model (cAMP pathway)
1. Extracellular hormone (1ᵗʳˢᵗ messenger) binds membrane receptor
2. Receptor activates G-protein complex (GDP→GTP exchange)
3. G-protein modulates adenylate cyclase activity → changes intracellular [cAMP]
4. cAMP (2ⁿᵈ messenger) activates protein kinases
5. Kinases phosphorylate target enzymes / membrane channels
6. Rapid, amplified cellular response
Termination
- Phosphodiesterase quickly degrades cAMP to AMP
- Ongoing effect requires continued hormone presence
Hormone examples: glucagon, prolactin, ACTH, LH, FSH, TSH, ADH, PTH, hypothalamic releasing factors

Alter organelle activity (e.g.
- ↑ mitochondria → ↑ ATP production
- ↑ ribosomes → ↑ protein synthesis)
Modify membrane permeability (e.g. ↑ glucose uptake via transporters)
Activate or inhibit metabolic pathways
Stimulate secretion (exocytosis)
Influence muscle contraction/relaxation

Effective endocrine signalling requires:
- Proper chemical classification → transport & receptor accessibility
- Correct communication mode (autocrine, paracrine, endocrine)
- Reversible binding when carrier proteins are involved
- Either direct gene modulation (lipid-soluble) or second-messenger cascades (water-soluble)
Failure at any step (synthesis, transport, receptor, messenger degradation) compromises homeostasis

Builds on basic cell‐membrane theory (diffusion, receptors) and neuronal communication (neurotransmitter vs hormone distinctions)
Reinforces pharmacology principles: drug lipophilicity parallels hormone solubility and receptor targeting
Links to systemic physiology chapters that follow: e.g. role of cortisol in stress, insulin/glucagon in metabolism (to be covered in later parts)

Knowing solubility class guides drug design (e.g. synthetic steroids vs peptide analogues)
Disorders
- Transport protein defects → abnormal free/bound hormone ratios (e.g. thyroid-binding-globulin deficiency)
- Receptor mutations → hormone resistance syndromes
Therapeutic interventions often mimic or block second-messenger pathways (e.g. β-adrenergic blockers ↓ cAMP)

Hormone manipulation (e.g. anabolic steroids) raises fairness & health issues in sports
Endocrine disruptors in environment (plastics, pesticides) challenge public-health policy

Lecturer: Dr Gary Whittaker – g.whittaker@curtin.edu.au
Primary Text: VanPutte, Regan & Russo, Seeley’s A&P 12^{th} ed., McGraw-Hill
Copyright Notice: Material reproduced under Part VB of the Australian Copyright Act 1968