H2-receptor antagonists are commonly prescribed antiulcer drugsin the United States. They include:
Cimetidine, nizatidine, and ranitidine are absorbed rapidly and completely from the GI tract. Famotidine isn’t completely ab-sorbed. Antacids may reduce the absorption of H2-receptor antag-onists.
H2-receptor antagonists are distributed widely throughout the body, metabolized by the liver, and excreted primarily in urine.
H2-receptor antagonists block histamine from stimulating the acid-secreting parietal cells of the stomach.
Acid secretion in the stomach depends on the binding of gastrin, acetylcholine, and histamine to receptors on the parietal cells. If the binding of one of these substances is blocked, acid secretion is reduced. The H2-receptor antagonists, by binding with H2 recep-tors, block the action of histamine in the stomach and reduce acid secretion. (See How H2-receptor antagonists work)
H2-receptor antagonists are used therapeutically to:
§ promote healing of duodenal and gastric ulcers
§ provide long-term treatment of pathologic GI hypersecretory conditions such as Zollinger-Ellison syndrome
§ reduce gastric acid production and prevent stress ulcers in the severely ill patient and in the patient with reflux esophagitis or up-per GI bleeding.
H2-receptor antagonists may interact with antacids and other drugs.
§ Antacids reduce the absorption of cimetidine, famotidine, nizati-dine, and ranitidine.
§ Cimetidine may increase the blood levels of oral anticoagulants, propranolol (and possibly other beta-adrenergic blockers), benzo-diazepines, tricyclic antidepressants, theophylline, procainamide, quinidine, lidocaine, phenytoin, calcium channel blockers, cyclo-sporine, carbamazepine, and opioid analgesics by reducing their metabolism in the liver and subsequent excretion.
§ Cimetidine taken with carmustine increases the risk of bone marrow toxicity.
§ Cimetidine inhibits metabolism of ethyl alcohol in the stomach, resulting in higher blood alcohol levels. (See Adverse reactions toH2-receptor antagonists.)