Morphine for the Treatment of Pain in Sickle Cell Disease

Figure 2

Proposed model of morphine activity in the kidney. Morphine stimulates cyclooxygenase-2 (COX-2), hemoxygenase-1 (HO-1), inducible/endothelial nitric oxide synthase (i/e NOS), oxidative stress via reactive oxygen species/peroxynitrite, mitogen activated protein kinase/extracellular signal regulated kinase (MAPK/ERK), platelet-derived growth factor receptor-β (PDGFR-β), and platelet-derived growth factor-BB (PDGF-BB). These molecular changes are accompanied by albuminuria and glomerular pathology in morphine treated mice. Together, these morphine-induced cellular, molecular, and pathological effects may stimulate and exacerbate existent renal damage in sickle cell disease.