Oxygen tension measurements in carotid body of the cat

Whalen, W. J.; Savoca, J; Nair, P.

doi:10.1152/ajplegacy.1973.225.4.986

Cited by 28 publications

(13 citation statements)

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“…In these experiments, we included environmental O 2 levels for each lung and cardiac ECs of 8 and 2.5%, respectively [31, 32]. When exposed to 2.5% O 2 there was an overall increased rate of proliferation in control lung ECs over normoxic conditions in BrDU incorporation experiments (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Inhibition of ARNT severely compromises endothelial cell viability and function in response to moderate hypoxia

et al. 2012

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Section: Resultsmentioning

confidence: 99%

“…S4A). To verify the requirement of ARNT in ECs, we isolated cardiac ECs which are considered to reside in a lower gradients of O 2 [32]. Cultures of control cardiac ECs also show that both 2.5 and 8% O 2 induce their proliferation (Figure S4A).…”

Section: Resultsmentioning

confidence: 99%

Inhibition of ARNT severely compromises endothelial cell viability and function in response to moderate hypoxia

et al. 2012

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“…Conflicting data regarding the tissue level of Po 2 in the carotid body has been reported. Thus, Acker and coworkers (12) obtained, using O 2 electrodes, remarkably low carotid body tissue Po 2 values of 7 to 20 mmHg at a Pao 2 of 100 mmHg, while the relatively sharper electrodes of Whalen and Nair (902, 905) revealed higher values of between 40 and 70 mmHg throughout the organ. An optical, noninvasive phosphorescence quenching technique, avoiding tissue damage, obtained a microvascular Po 2 value of 23 mmHg with equilibrated saline perfusion in vitro (757), but with blood perfusion in vivo , at a Pao 2 of 103 mmHg, this value increased to a relatively normal to high, microvascular Po 2 of 53 mmHg (502).…”

Section: Sensing Hypoxia—the Stimulusmentioning

confidence: 99%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

465

572

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The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

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“…According to the experimental data, the РО 2 level in the normoxic perfusate (under natural conditions, arterial blood), at which a basal level of the electrical activity of the SCN is observed, is approximately 125 mm Hg, while РО 2 in the microvascular bed is equal to 45 mm Hg [6], intratissue РО 2 is 40 mm Hg [7], and intracellular РО 2 is approximately 25 mm Hg [8]. Whalen et al [10] reported that chemoreceptor CB cells in vivo generated responses with decreases in РО 2 in tissues from 40 to 5-10 mm Hg. Whalen et al [10] reported that chemoreceptor CB cells in vivo generated responses with decreases in РО 2 in tissues from 40 to 5-10 mm Hg.…”

Section: Carotid Bodies (Cb)mentioning

confidence: 98%