prostaglandines

Prostaglandins, or prostanoids, are a group of biologically active lipid compounds derived from arachidonic acid. They belong to the larger family of eicosanoids and function mainly as local mediators (paracrine and autocrine signals) that regulate inflammation, vascular tone, smooth muscle activity, and other physiological processes.

Biosynthesis and metabolism occur on demand. Arachidonic acid is released from membrane phospholipids by phospholipase A2, then converted by cyclooxygenase enzymes (COX-1 and COX-2) to prostaglandin G2 and H2 (PGH2). PGH2 is subsequently transformed by specific synthases into different prostaglandins, including PGE2, PGD2, PGF2alpha, and PGI2 (prostacyclin). Prostaglandins act through G protein–coupled receptors: PGE2 operates via EP1–EP4 receptors, PGD2 via DP receptors, PGF2alpha via FP receptors, and PGI2 via IP receptors. Thromboxane A2, while related, engages its own receptor (TP) and is sometimes discussed alongside prostaglandins in cardiovascular contexts. Prostaglandins are rapidly metabolized and have short half-lives, limiting their actions to the immediate vicinity of production.

Physiological and clinical roles are diverse. They modulate pain and fever during inflammation, influence vascular tone and permeability, and regulate uterine contractions (notably PGF2alpha). In the kidney, they affect glomerular filtration and salt balance. Clinically, NSAIDs inhibit COX enzymes to reduce prostaglandin synthesis. Therapeutic prostaglandins or analogs include misoprostol (PGE1) for gastric protection, dinoprostone (PGE2) for cervical ripening, alprostadil (PGE1) to maintain ductus arteriosus, epoprostenol (prostacyclin) for pulmonary arterial hypertension, and latanoprost (a PGF2alpha analog) for glaucoma. Adverse effects can include GI irritation, bleeding risk, and fluid retention, reflecting their broad biological actions.