Carotid body chemoreceptors sensing hypoxia and hypercapnia signal the body to produce erythropoietin (EPO) to stimulate red blood cell production.
"there's these little chemoreceptors, I think they're somewhere around the carotid artery, and they will sense that phenomenon and give your body a signal to create this protein called EPO, erythropoietin, to essentially activate the production of red blood cells." (said at 0:37:29)
The speaker misattributes the physiological sensor for erythropoietin (EPO) production to the carotid body chemoreceptors. While peripheral chemoreceptors located at the carotid bifurcation (the carotid bodies) sense hypoxia, hypercapnia, and acidosis, their primary function is to signal the brainstem to regulate ventilation and cardiovascular reflexes, not to stimulate EPO production. EPO synthesis is predominantly regulated directly within the kidneys (by interstitial peritubular cells) and liver via cell-autonomous oxygen-sensing pathways mediated by prolyl hydroxylase domain proteins and hypoxia-inducible factors (HIF-1/HIF-2).
- contradicts: Hypoxia-induced erythropoietin production: a paradigm for oxygen-regulated gene expression… (Clinical and experimental pharmacology & physiology 2006)
"In addition to the tight regulation by oxygen tension, temporal and tissue-specific signals limit expression of the EPO gene primarily to the fetal liver and the adult kidney." (abstract, passage verified)
pubmedfull study (doi) - contradicts: Hypoxic regulation of erythropoiesis and iron metabolism. (American journal of physiology. Renal physiology 2010)
"The kidney is a highly sensitive oxygen sensor and plays a central role in mediating the hypoxic induction of red blood cell production. Efforts to understand the molecular basis of oxygen-regulated erythropoiesis have led to the identification of erythropoietin (EPO), which is essential for normal erythropoiesis and to the purification of hypoxia-inducible factor (HIF), the transcription factor that regulates EPO synthesis and mediates cellular adaptation to hypoxia." (abstract, passage verified)
pubmedfull study (doi)