Topic 9 — Prostaglandins: Biological Actions and Clinical Applications

Connect prostaglandin synthesis, receptor actions, organ effects and clinical uses for rapid revision.

1. THE TOPIC IN ONE CONNECTED FLOW

Prostaglandins are locally acting lipid mediators formed from arachidonic acid. Their effects depend on which prostanoid is produced and which receptor subtype is present in the target tissue. This explains how one pathway can influence inflammation, vascular tone, platelets, the uterus, kidneys, eye and several therapeutic responses.

Cell Stimulation

Membrane phospholipids are activated

→

Arachidonic Acid

Released from cell membranes

→

Cyclooxygenase

Forms prostaglandin intermediates

→

Specific Prostanoids

PGE₂, PGF₂α, PGD₂, PGI₂, TXA₂

→

GPCR Binding

EP, FP, DP, IP or TP receptors

→

Second Messengers

Changes in cAMP or intracellular calcium

→

Organ Response

Vascular, platelet, inflammatory or smooth-muscle effect

Two major functional branches

PGI₂ from endothelium
→ vasodilation → reduced platelet activation → protection against excessive thrombosis

TXA₂ from activated platelets
→ vasoconstriction → platelet aggregation → support of hemostatic plug formation

2. KEY CLINICAL CONNECTIONS

Inflammation → Pain and Fever

PGE₂ → sensitizes peripheral nociceptors → hyperalgesia.

PGE₂ in hypothalamus → raises thermoregulatory set point → fever.

Uterus → Therapeutic Use

PGE compounds → cervical ripening + uterine activity → induction-related use.

PGF₂α analogue → strong uterine contraction → useful when a marked uterotonic effect is required.

Eye and Ductus Arteriosus

Latanoprost → increased uveoscleral outflow → reduced intraocular pressure.

Alprostadil → ductal smooth-muscle relaxation → maintenance of ductus arteriosus patency.

3. AIM HIGH-YIELD INTEGRATION REVIEW

⭐ Arachidonic acid → cyclooxygenase → prostanoids: this is the central synthesis pathway linking cell stimulation to prostaglandin effects.

⭐ Different GPCR subtypes → different second messengers → different organ responses: this explains why prostaglandins may contract one tissue but relax another.

PGE₂ → nociceptor sensitization + hypothalamic set-point elevation → inflammatory pain and fever.

PGE₂ and PGI₂ → vasodilation → increased local blood flow → redness and warmth during inflammation.

⭐ Endothelial PGI₂ → vasodilation + platelet inhibition, while platelet TXA₂ → vasoconstriction + aggregation.

Renal PGE₂/PGI₂ → local vasodilation → support of renal perfusion when vasoconstrictor influences are present.

Misoprostol → gastric protection + uterine effects; dinoprostone → cervical ripening; carboprost → strong uterine contraction.

⭐ Latanoprost → increased aqueous outflow → lower intraocular pressure, while alprostadil → maintained ductal patency.

AIM Exam Trap:
Do not confuse PGI₂ with TXA₂: PGI₂ inhibits platelet aggregation and dilates vessels, whereas TXA₂ promotes aggregation and vasoconstriction.