Triggering of erythropoietin production by hypoxia is inhibited by respiratory and metabolic acidosis
Autor: | Kai-Uwe Eckardt, Armin Kurtz, Christian Bauer |
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Rok vydání: | 1990 |
Předmět: |
Male
medicine.medical_specialty Physiology Hypoxic hypoxia 610 Medizin Metabolic alkalosis Acidosis Respiratory/metabolism Mice Anoxia/metabolism Erythropoietin/biosynthesis Physiology (medical) Internal medicine medicine Animals 570 Biowissenschaften Biologie Hypoxia Erythropoietin Acidosis Acid-Base Equilibrium Carbon Monoxide ddc:610 Chemistry Metabolic acidosis Hydrogen-Ion Concentration Hypoxia (medical) medicine.disease Respiratory acidosis Endocrinology Acidosis/metabolism Acidosis Respiratory ddc:570 medicine.symptom Hypercapnia medicine.drug |
Zdroj: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 258:R678-R683 |
ISSN: | 1522-1490 0363-6119 |
DOI: | 10.1152/ajpregu.1990.258.3.r678 |
Popis: | Erythropoietin (EPO) production in response to hypoxic hypoxia is known to be attenuated by simultaneous hypercapnia. This study aimed to investigate whether this inhibitory effect of hypercapnia is 1) a direct effect of carbon dioxide or mediated by changes in pH or bicarbonate, 2) affects also carbon monoxide hypoxia, and 3) influences either the synthesis and release of EPO or the mechanisms by which hypoxia triggers an increase in EPO production rate. We found that EPO formation in mice exposed to normobaric hypoxia (8% O2) or to carbon monoxide (0.1%) was reduced by 30 and 42% when animals were simultaneously exposed to hypercapnia (7% CO2), by 35 and 38% when subjected to metabolic acidosis (NH4Cl), and unchanged when subjected to metabolic alkalosis (NaHCO3). In animals exposed to brief hypoxia (15 min) and subsequent normoxia (2 h), metabolic acidosis did not affect EPO levels when initiated after the hypoxic period. The results indicate that acidosis inhibits hypoxia-induced triggering of EPO formation independently of PCO2 and HCO3 levels. Because this inhibitory effect is also present during carbon monoxide hypoxia, it appears not solely due to potentiated hyperpnea. Alternatively, it may result from a facilitated intrarenal oxygen release or a direct effect at the EPO production sites. |
Databáze: | OpenAIRE |
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