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Pharmacology: Pharmacodynamics: Domperidone is a dopamine receptor (D2) antagonist. Domperidone is a selective peripheral dopamine antagonist at the D2 dopamine receptor in the Chemo-receptor Trigger Zone (CTZ) and stomach. Domperidone does not readily enter the central nervous system (the chemoreceptor trigger zone is considered to lie outside the blood-brain barrier). Domperidone increases spontaneous gastric activity and antagonizes dopamine inhibition of gastric emptying. Domperidone has been shown to increase lower esophageal sphincter pressure and promotes esophageal and antral peristalsis and also increases pyloric dilatation. Domperidone increases the frequency, amplitude, and duration of duodenal contraction and reduces the small bowel transit time. Domperidone has no acetylcholine-like effect.
Pharmacokinetics: Absorption: Domperidone is rapidly absorbed after oral administration occurring at approximately 1hr after dosing. Domperidone's bioavailability is enhanced in normal subjects when taken after a meal, patients with gastro-intestinal complaints should take Domperidone 15-30 minutes before meal as reduced gastric acidity impairs absorption of Domperidone.
Distribution: Domperidone is bound to plasma proteins.
Metabolism: Domperidone goes through rapid and extensive hepatic metabolism by hydroxylation and N dealkylation. In vitro metabolism experiments revealed that CYP3A4, a major form of cytochrome P-450, is involved in N-dealkylation while CYP3A4, CYP1A2 and CYP2E1 is involved in aromatic hydroxylation.
Excretion: Domperidone is eliminated in the urine and fecal excretions 7-9 hours after oral administration.
