Prostaglandin synthesis by rat glomerular mesangial cells in culture.
The long¬term renal toxicity of NSAIDs may be caused by ..
Figure 3. Pathogenesis of gastric damage by NSAIDs. Current evidence indicates that the majority of harmful effects mediated by NSAIDs result from inhibition of the synthesis of mucosal-protective prostaglandins produced by constitutive COX-1 activity. Direct drug-mediated irritant effects on epithelial cells appear to play only a minor role in GI toxicity. The presence of infections by the bacterium H pylori represents a separate risk factor that increases the likelihood of developing duodenal ulcers (Feldman, 2014).
Mechanisms of NSAID Induced Functional Renal Toxicity
NSAIDs work by suppressing the production of prostaglandins. Prostaglandins are chemical messengers that mediate inflammation, fever and the sensation of pain. NSAIDs block the production of prostaglandins by inhibiting the action of an enzyme, cyclooxygenase (COX). This enzyme is responsible for converting precursor acids into prostaglandins.
NSAIDs block the synthesis of prostaglandin G 2.
NSAIDs-induced hypertension is due to the effects on renal function. Specifically, NSAIDs cause dose-related increases in sodium and water retention. In addition, NSAID use may reduce the effect of antihypertensive drugs except calcium channel blockers.