Dr. William G. Paterson
B.Sc., M.D., FRCPC
Chief, Division of Gastroenterology

Department of Medicine
Cross appointments: Dept. of Physiology, Dept. of Biology

Office Tel: 613 544-3400 ext. 2292
patersow@hdh.kari.net



Welcome
to the
Paterson Lab


The main focus of Dr. Paterson’s research program is the study of the physiology and pathophysiology of the esophagus. Using a spectrum of methodologies ranging from whole organ motility recordings to single cell intracellular and patch clamp recordings, his CIHR-funded research explores the neuromuscular mechanisms that control esophageal peristalsis and lower esophageal sphincter (LES) tone and relaxation. His laboratory has been able to define an important role for calcium-activated chloride channels in the maintenance of resting LES tone and LES relaxation induced by neural release of nitric oxide. More recently, they have discovered that Interstitial cells of Cajal are not required for normal nitrergic neurotransmission in the LES, a hypothesis that up to now has gained widespread acceptance.

Dr. Paterson’s lab is also interested in how inflammation alters gut neuromuscular function. Using a model of reflux esophagitis, his lab has made novel discoveries on the role of mast cell-derived mediators in the neuromuscular dysfunction that complicates esophagitis. They have evidence that mast cell-derived inflammatory mediators induce long axis esophageal shortening by causing contraction of the longitudinal muscle layer, probably via the release of Substance P or other neurokinins. This may have important clinical relevance with respect to the etiology of hiatus hernia and esophageal pain syndromes. More recently, studies have begun to elucidate the abnormalities in neuromuscular function that are associated with colitis. The goal of these studies is to ultimately provide better therapy for the pain and diarrhea associated with inflammatory bowel diseases.

In parallel, Dr. Paterson conducts a number of clinical projects in humans, focused mainly on gastroesophageal reflux disease and functional motor and sensory disorders of the GI tract.