Kidney Regulation of Erythropoietin Production
Hypoxia is the fundamental stimulus for erythropoietin (Ep) production (Fisher 1983, 1988; Kurz et al. 1986). Our model for kidney Ep production postulates that an oxygen deficit initiates a cascade of events which lead to increased biosynthesis and secretion of Ep. The physiologic and pathophysiologic control involved is still not clearly understood. However, there is a primary oxygen-sensing reaction in the kidney which is triggered by a reduction in ambient partial pressure of oxygen (high altitude, hypobaria); a decreased passage of oxygen across the pulmonary endothelium (obstructive lung disease); a decrease in the oxygen-carrying capacity of hemoglobin (anemia); a decrease in oxygen utilization by the kidney (cobalt) (Fisher and Birdwell 1961); and a decrease in the flow of blood to the kidney (renal artery constriction, atherosclerosis, thrombosis).
KeywordsHepG2 Cell Adenylate Cyclase Cholera Toxin Hep3B Cell Ischemic Hypoxia
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- Berridge MJ (1984) Inositol triphosphate and diacylglycerol as second messengers. SOD Biochem J 222:345–360Google Scholar
- Fisher JW (1991) Regulation of erythropoietin (Ep) production. In: Handbook of renal physiology. Oxford University Press, New York (in press)Google Scholar
- Paul P, Rothmann SA, Meagher RC (1988) Modulation of erythropoietin production by adenosine. J Lab CHn Med 112:168–173Google Scholar