Developmental changes of blood oxygen pressure are instrumental for the regulation of blood oxygen affinity (via ATP/2,3-diphosphoglycerate (2,3-DPG) concentration) and carbonic anhydrase (CA) synthesis in red cells of chick embryos. Hypoxia is the physiological stimulus for the coordinated onset of synthesis of CA and 2,3-DPG in late chick embryos, whereas the higher blood oxygen pressure prevailing in early—and midterm embryos suppresses CA and 2,3-DPG synthesis and increases red cell ATP. This mechanism guarantees flexible adaption of the oxygen affinity to the prevailing oxygen pressure. At least two hormonal effectors seem to be involved in the PO2-dependent regulation: (a) a heat-labile, low molecular weight compound of embryonic chick plasma that stimulates CA and 2,3-DPG synthesis and (b) an antagonistically-acting, short-lived metabolite present in the blood of normoxic and hyperoxic embryos, whose activity/concentration should be reduced with falling PO2. While the identity of the CAII inducer is not yet known, extracellular ATP is a likely candidate for the role of antagonist. In vitro it depresses CAII synthesis via activation of phospholipase C, and—by a different transduction pathway—stimulates net synthesis of ATP and downregulation of 2,3-DPG levels.
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Developmental changes of blood oxygen pressure are instrumental for the regulation of blood oxygen affinity (via ATP/2,3-diphosphoglycerate (2,3-DPG) concentration) and carbonic anhydrase (CA) synthesis in red cells of chick embryos. Hypoxia is the physiological stimulus for the coordinated onset of synthesis of CA and 2,3-DPG in late chick embryos, whereas the higher blood oxygen pressure prevailing in early—and midterm embryos suppresses CA and 2,3-DPG synthesis and increases red cell ATP. This mechanism guarantees flexible adaption of the oxygen affinity to the prevailing oxygen pressure. At least two hormonal effectors seem to be involved in the PO2-dependent regulation: (a) a heat-labile, low molecular weight compound of embryonic chick plasma that stimulates CA and 2,3-DPG synthesis and (b) an antagonistically-acting, short-lived metabolite present in the blood of normoxic and hyperoxic embryos, whose activity/concentration should be reduced with falling PO2. While the identity of the CAII inducer is not yet known, extracellular ATP is a likely candidate for the role of antagonist. In vitro it depresses CAII synthesis via activation of phospholipase C, and—by a different transduction pathway—stimulates net synthesis of ATP and downregulation of 2,3-DPG levels.
| All Time | Past 365 days | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 126 | 29 | 4 |
| Full Text Views | 7 | 0 | 0 |
| PDF Views & Downloads | 7 | 0 | 0 |