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Regulation of oxygen sensing in peripheral arterial chemoreceptors
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Regulation of oxygen sensing in peripheral arterial chemoreceptors

Sukhamay Lahiri, Charmaine Rozanov, Arijit Roy, Bayard Storey and Donald G Buerk
International Journal of Biochemistry and Cell Biology, v 33(8), pp 755-774
2001
PMID: 11404180

Abstract

Acute hypoxia Calcium Carotid body Chronic hypoxia CO and NO sensing Glomus cells Hypoxia inducible factors Ion channel hypothesis Mitochondrial respiration Nerve endings Neurotransmitters Normoxic protein degradation Potassium channels Ventilation
The carotid bodies are a small pair of highly vascularized and well perfused organs located at each carotid artery bifurcation, strategically situated to sense oxygen in arterial blood as it leaves the heart. Carotid body glomus cells are identified as the primary oxygen sensors, which respond to changes in blood P O 2 within milliseconds. Acute hypoxia causes a rapid increase in carotid sinus nerve (CSN) activity, providing afferent signals to the respiratory center in the brainstem. Glomus cells secrete numerous neurotransmitters that modulate CSN firing rates. This review will discuss major hypotheses that have emerged regarding acute oxygen sensing by glomus cells. In contrast, chronic responses to hypoxia are much slower, involving cytosolic reactions that take place over several minutes and nuclear reactions which occur over several hours. Converging concepts from different areas of research in oxygen sensing cells and tissues (including the carotid body) have been combined to describe molecular and biochemical changes that take place in the carotid body with chronic hypoxia. These include oxygen dependent proteolytic processes in the cytosol and gene transcription in the nucleus. In addition, cellular and nuclear responses to chronic hypoxia will be discussed.

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Web of Science research areas
Biochemistry & Molecular Biology
Cell Biology
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