Ranitidine Hydrochloride (AH19065) is a member of the class of histamine H2-receptor antagonists with antacid activity. Ranitidine is a competitive and reversible inhibitor of the action of histamine, released by enterochromaffin-like (ECL) cells, at the histamine H2-receptors on parietal cells in the stomach, thereby inhibiting the normal and meal-stimulated secretion of stomach acid. In addition, other substances that promote acid secretion have a reduced effect on parietal cells when the H2 receptors are blocked.

Ranitidine sensitizes hepatocytes to killing by cytotoxic products from activated neutrophils, whereas Famotidine lacks this ability. [1] Ranitidine inhibits the production of tumor necrosis factor-alpha (TNF-alpha) in monocytes stimulated with lipopolysaccharide in vitro. [2] Ranitidine reduces the Kel of morphine dose-dependently with a maximum effect of 50%, and increases the relative concentration of morphine-6-glucuronide to morphine-3-glucuronide in isolated guinea pig hepatocytes. Ranitidine gradually decreases the morphine-3-glucuronide/morphine-6-glucuronide ratio by up to 21%. [3]

Ranitidine results in liver injury as evidence by increased in serum alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transferase activities within 6 hours after Ranitidine administration in rats. [1] Ranitidine inhibits hepatic ischemia/reperfusion-induced increase in hepatic tissue levels of TNF-alpha, cytokine-induced neutrophil chemoattractant, and hepatic accumulation of neutrophils in rats. [2] Ranitidine cotreatment enhances LPS-induced coagulation prior to liver injury, and anticoagulants reduce liver damage in LPS/RAN-treated rats. Ranitidine /LPS-treated rats results in the formation of fibrin clots in liver sinusoids, and prevention of fibrin deposition associated with reduced hepatocellular injury. Ranitidine cotreatment enhances the LPS-induced TNF increase before the onset of hepatocellular injury in rats. [4] Ranitidine displays anxiolytic effects in the elevated plus-maze as indicated by an increase in time spent in the open arms, more open-arm scanning and more end-excursions in rats. [5]