Triggering of erythropoietin production by hypoxia is inhibited by respiratory and metabolic acidosis
| العنوان: | Triggering of erythropoietin production by hypoxia is inhibited by respiratory and metabolic acidosis |
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| المؤلفون: | Kai-Uwe Eckardt, Armin Kurtz, Christian Bauer |
| المصدر: | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 258:R678-R683 |
| بيانات النشر: | American Physiological Society, 1990. |
| سنة النشر: | 1990 |
| مصطلحات موضوعية: | 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 |
| الوصف: | 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. |
| وصف الملف: | application/pdf |
| تدمد: | 1522-1490 0363-6119 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ff7f9469bb65db1659338dc73d889bfdTest https://doi.org/10.1152/ajpregu.1990.258.3.r678Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....ff7f9469bb65db1659338dc73d889bfd |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15221490 03636119 |
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