GERD Mechanisms: LES Dysfunction

The lower esophageal sphincter (LES) is a 3-4 cm zone of specialized smooth muscle at the gastroesophageal junction that maintains tonic contraction at 10-30 mmHg resting pressure through intrinsic myogenic tone modulated by excitatory (acetylcholine, substance P) and inhibitory (nitric oxide, vasoactive intestinal peptide) neurotransmitters. LES dysfunction occurs through several distinct mechanisms. Transient LES relaxations (TLESRs) are the most common: vagal afferent mechanoreceptors in the gastric cardia detect distension and trigger a vagovagal reflex that releases nitric oxide from inhibitory neurons in the myenteric plexus, causing LES relaxation lasting 10-60 seconds — unlike swallow-induced relaxation, TLESRs are not preceded by esophageal peristalsis, so refluxed material is not cleared. Chronically hypotensive LES (resting pressure <10 mmHg) allows free reflux during episodes of increased intra-abdominal pressure (coughing, straining, bending). Scleroderma causes irreversible LES incompetence through progressive fibrotic replacement of smooth muscle, producing aperistalsis and severe reflux. Hiatal hernia disrupts LES function by displacing the sphincter above the crural diaphragm, eliminating the extrinsic compression that augments LES pressure; it also creates a hernia sac that traps acid above the diaphragm (the acid pocket)...