Hepatic and renal erythropoietin production during various intervals of short-term hypoxia.
Hypoxia stimulates erythropoietin (Ep) production and subsequent stimulation of erythropoiesis. Chronically applied hypoxia results in a variety of physiological alterations including polycythemia, hemoglobinemia, and vascular and metabolic changes. As red cell mass increases to such an extent to allow for adequate tissue oxygenation, plasma Ep levels drop and the rate of erythropoiesis is lowered. In the present work, the precise contribution of the kidney and the liver to the Ep response to acutely administered hypoxia (6-24 hr/0.4 atm) was determined using an in situ tandem perfusion of the liver and kidneys. The results indicate that hepatic and renal Ep production during different intervals of acute hypoxia is not uniform. This alteration may be partially explained by the reported reduction in splanchnic blood flow and a possible redistribution of hepatic microcirculation, which may cause the liver to become more hypoxic than the kidney under the same ambient pO2. The role of the liver becomes more pronounced as the time of acute hypoxic exposure increases, whereas the Ep content of renal perfusates is not drastically altered. At certain intervals during hypoxia, the liver displays a greater potential to elaborate Ep.
D000818:Animals; D004921:Erythropoietin / Q000096:biosynthesis* / Q000097:blood; D000860:Hypoxia / Q000378:metabolism* / Q000473:pathology; D007668:Kidney / Q000378:metabolism*; D007700:Kinetics; D008099:Liver / Q000378:metabolism* / Q000473:pathology; D008264:Macrophages / Q000473:pathology; D008297:Male; D051381:Rats
D004921:Erythropoietin