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Arterial Chemoreceptors in Physiology and Pathophysiology

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Cover of 'Arterial Chemoreceptors in Physiology and Pathophysiology'

Table of Contents

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    Book Overview
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    Chapter 1 Epigenetic Regulation of Carotid Body Oxygen Sensing: Clinical Implications.
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    Chapter 2 Experimental Observations on the Biological Significance of Hydrogen Sulfide in Carotid Body Chemoreception
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    Chapter 3 The CamKKβ Inhibitor STO609 Causes Artefacts in Calcium Imaging and Selectively Inhibits BKCa in Mouse Carotid Body Type I Cells
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    Chapter 4 Tissue Dynamics of the Carotid Body Under Chronic Hypoxia: A Computational Study
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    Chapter 5 Paracrine Signaling in Glial-Like Type II Cells of the Rat Carotid Body.
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    Chapter 6 Selective mu and kappa Opioid Agonists Inhibit Voltage-Gated Ca2+ Entry in Isolated Neonatal Rat Carotid Body Type I Cells
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    Chapter 7 Measurement of ROS Levels and Membrane Potential Dynamics in the Intact Carotid Body Ex Vivo.
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    Chapter 8 Acutely Administered Leptin Increases [Ca(2+)] i and BK Ca Currents But Does Not Alter Chemosensory Behavior in Rat Carotid Body Type I Cells.
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    Chapter 9 Functional Properties of Mitochondria in the Type-1 Cell and Their Role in Oxygen Sensing
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    Chapter 10 Potentiation of Hypoxic Pulmonary Vasoconstriction by Hydrogen Sulfide Precursors 3-Mercaptopyruvate and D-Cysteine Is Blocked by the Cystathionine γ Lyase Inhibitor Propargylglycine.
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    Chapter 11 Modulation of the LKB1-AMPK Signalling Pathway Underpins Hypoxic Pulmonary Vasoconstriction and Pulmonary Hypertension
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    Chapter 12 Organismal Responses to Hypoxemic Challenges.
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    Chapter 13 Effect of Lipopolysaccharide Exposure on Structure and Function of the Carotid Body in Newborn Rats.
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    Chapter 14 Hypoxic Ventilatory Reactivity in Experimental Diabetes.
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    Chapter 15 Adenosine Receptor Blockade by Caffeine Inhibits Carotid Sinus Nerve Chemosensory Activity in Chronic Intermittent Hypoxic Animals.
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    Chapter 16 Neurotrophic Properties, Chemosensory Responses and Neurogenic Niche of the Human Carotid Body.
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    Chapter 17 Is the Carotid Body a Metabolic Monitor?
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    Chapter 18 Lipopolysaccharide-Induced Ionized Hypocalcemia and Acute Kidney Injury in Carotid Chemo/Baro-Denervated Rats
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    Chapter 19 Role of the Carotid Body Chemoreflex in the Pathophysiology of Heart Failure: A Perspective from Animal Studies
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    Chapter 20 A Short-Term Fasting in Neonates Induces Breathing Instability and Epigenetic Modification in the Carotid Body.
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    Chapter 21 Carotid Body Chemoreflex Mediates Intermittent Hypoxia-Induced Oxidative Stress in the Adrenal Medulla.
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    Chapter 22 The Association Between Antihypertensive Medication and Blood Pressure Control in Patients with Obstructive Sleep Apnea
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    Chapter 23 An Overview on the Respiratory Stimulant Effects of Caffeine and Progesterone on Response to Hypoxia and Apnea Frequency in Developing Rats.
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    Chapter 24 Hyperbaric Oxygen Therapy Improves Glucose Homeostasis in Type 2 Diabetes Patients: A Likely Involvement of the Carotid Bodies.
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    Chapter 25 Possible Role of TRP Channels in Rat Glomus Cells.
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    Chapter 26 Nitric Oxide Deficit Is Part of the Maladaptive Paracrine-Autocrine Response of the Carotid Body to Intermittent Hypoxia in Sleep Apnea.
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    Chapter 27 Respiratory Control in the mdx Mouse Model of Duchenne Muscular Dystrophy.
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    Chapter 28 Mild Chronic Intermittent Hypoxia in Wistar Rats Evokes Significant Cardiovascular Pathophysiology but No Overt Changes in Carotid Body-Mediated Respiratory Responses.
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    Chapter 29 Crucial Role of the Carotid Body Chemoreceptors on the Development of High Arterial Blood Pressure During Chronic Intermittent Hypoxia.
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    Chapter 30 Relative Contribution of Nuclear and Membrane Progesterone Receptors in Respiratory Control.
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    Chapter 31 Inhibition of Protein Kinases AKT and ERK1/2 Reduce the Carotid Body Chemoreceptor Response to Hypoxia in Adult Rats.
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    Chapter 32 Ecto-5′-Nucleotidase, Adenosine and Transmembrane Adenylyl Cyclase Signalling Regulate Basal Carotid Body Chemoafferent Outflow and Establish the Sensitivity to Hypercapnia
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    Chapter 33 T-Type Ca2+ Channel Regulation by CO: A Mechanism for Control of Cell Proliferation
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    Chapter 34 Glutamatergic Receptor Activation in the Commisural Nucleus Tractus Solitarii (cNTS) Mediates Brain Glucose Retention (BGR) Response to Anoxic Carotid Chemoreceptor (CChr) Stimulation in Rats.
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    Chapter 35 Augmented 5-HT Secretion in Pulmonary Neuroepithelial Bodies from PHD1 Null Mice.
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    Chapter 36 Selective Expression of Galanin in Neuronal-Like Cells of the Human Carotid Body.
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    Chapter 37 Role of BK Channels in Murine Carotid Body Neural Responses in vivo.
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    Chapter 38 Chronic Intermittent Hypoxia Blunts the Expression of Ventilatory Long Term Facilitation in Sleeping Rats.
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    Chapter 39 Heme Oxygenase-1 Influences Apoptosis via CO-mediated Inhibition of K(+) Channels.
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    Chapter 40 Inhibition of T-type Ca(2+) Channels by Hydrogen Sulfide.
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    Chapter 41 GAL-021 and GAL-160 are Efficacious in Rat Models of Obstructive and Central Sleep Apnea and Inhibit BKCa in Isolated Rat Carotid Body Glomus Cells.
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    Chapter 42 The Human Carotid Body Gene Expression and Function in Signaling of Hypoxia and Inflammation.
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    Chapter 43 The Carotid Body Does Not Mediate the Acute Ventilatory Effects of Leptin.
Attention for Chapter 18: Lipopolysaccharide-Induced Ionized Hypocalcemia and Acute Kidney Injury in Carotid Chemo/Baro-Denervated Rats
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Chapter title
Lipopolysaccharide-Induced Ionized Hypocalcemia and Acute Kidney Injury in Carotid Chemo/Baro-Denervated Rats
Chapter number 18
Book title
Arterial Chemoreceptors in Physiology and Pathophysiology
Published in
Advances in experimental medicine and biology, January 2015
DOI 10.1007/978-3-319-18440-1_18
Pubmed ID
Book ISBNs
978-3-31-918439-5, 978-3-31-918440-1
Authors

R. Fernández, P. Cortés, R. Del Rio, C. Acuña-Castillo, E. P. Reyes

Abstract

The acute kidney injury (AKI) observed during sepsis is due to an uncontrolled release of inflammatory mediators. Septic patients develop electrolytic disturbances and one of the most important is ionized hypocalcemia. AKI adversely affects the function of other organs and hypocalcemia is associated with cardiovascular and respiratory dysfunctions. Since carotid body chemoreceptors modulate the systemic inflammatory response during sepsis syndromes, we used pentobarbitone-anesthetized male Sprague-Dawley rats in control condition (SHAM surgery) and after bilateral carotid neurotomy (carotid chemo/baro-denervated, BCN). We evaluate serum creatinine (CRE), serum neutrophil gelatinase-associated lipocaline (NGAL), ionized calcium (iCa) and cardiac Troponin I (cTnI) 90 min after the IP administration of 15 mg/kg lipopolysaccharide (LPS) or saline. In the SHAM group, LPS failed to induce significant changes CRE, NGAL, or iCa, and increased cTnI. Conversely, in the BCN group LPS increased CRE and NGAL, decreased iCa, and enhanced the increase of cTnI. Our results suggest that carotid chemo/baro-receptors might contribute to the regulation of both renal function and calcemia during sepsis. In addition, results imply that the carotid chemo-baroreceptors serve as an immunosensory organ.

Mendeley readers

The data shown below were compiled from readership statistics for 9 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 9 100%

Demographic breakdown

Readers by professional status Count As %
Professor > Associate Professor 3 33%
Student > Bachelor 1 11%
Researcher 1 11%
Other 1 11%
Unknown 3 33%
Readers by discipline Count As %
Agricultural and Biological Sciences 3 33%
Nursing and Health Professions 1 11%
Immunology and Microbiology 1 11%
Engineering 1 11%
Unknown 3 33%