Autacoids and Their Classification: Therapeutic Significance of Prostaglandins

Autacoids are biologically active substances produced within the body that generally act locally near their site of synthesis. They are often called local hormones because they regulate various physiological and pathological processes, including inflammation, pain, allergic reactions, vascular tone, gastric secretion and smooth muscle contraction. Understanding autacoids is essential for students preparing for pharmacy competitive examinations such as UPSC Drug Inspector, GPAT, NIPER, AIIMS Pharmacist, Railway Pharmacist, SSC, ESIC and State Pharmacist examinations.

Classification of Autacoids

Autacoids are broadly classified into four major groups: biogenic amines, lipid-derived mediators, peptide autacoids and other lipid mediators. Biogenic amines include histamine and serotonin (5-HT). Lipid-derived mediators include prostaglandins, thromboxanes and leukotrienes. Peptide autacoids include bradykinin, angiotensin II and substance P. Platelet-activating factor (PAF) is another important mediator involved in inflammation and platelet activation.

Prostaglandins and Their Therapeutic Significance

Prostaglandins are eicosanoids synthesized from arachidonic acid through the cyclooxygenase (COX) pathway. They participate in inflammation, pain, fever, gastric mucosal protection, renal function, platelet regulation and reproductive processes. Different prostaglandins produce different effects depending on the receptors present in target tissues.

Several prostaglandin analogues have important therapeutic applications. Misoprostol, a PGE₁ analogue, helps prevent NSAID-induced gastric ulcers. Dinoprostone (PGE₂) is used for cervical ripening, while carboprost, a PGF₂α analogue, is used in selected cases of postpartum haemorrhage. Alprostadil (PGE₁) maintains ductus arteriosus patency in selected neonates, whereas latanoprost, a PGF₂α analogue, reduces intraocular pressure in glaucoma. Epoprostenol, a prostacyclin (PGI₂) analogue, is used in pulmonary arterial hypertension.

Prostaglandin synthesis inhibitors, particularly non-steroidal anti-inflammatory drugs (NSAIDs), reduce pain, fever, and inflammation by inhibiting cyclooxygenase enzymes. Aspirin additionally reduces platelet thromboxane A₂ synthesis, thereby inhibiting platelet aggregation. Knowledge of these mediators, their receptors, therapeutic uses, and adverse effects is crucial for solving pharmacology MCQs and understanding rational drug therapy. Click the link below for more details.

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