Keywords:
Cellular signal transduction.
;
Gases -- Physiological effect.
;
Electronic books.
Description / Table of Contents:
This richly illustrated expert review of the biological, pharmacological and medical functions of the signaling molecules nitric oxide, carbon monoxide, and hydrogen sulfide collates the impressive quantity of fresh data accumulated in recent years.
Type of Medium:
Online Resource
Pages:
1 online resource (208 pages)
Edition:
1st ed.
ISBN:
9783642303388
URL:
https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=994562
Language:
English
Note:
Intro -- Gasotransmitters:Physiology and Pathophysiology -- Preface -- Contents -- 1 Nitric Oxide: Biological Synthesis and Functions -- Abstract -- 1.1…Introduction -- 1.2…Three Mammalian Isoforms of NOS -- 1.2.1 Basic Characteristics of the Three Isozymes -- 1.2.2 Structural and Mechanistic Aspects of NO Synthesis -- 1.2.3 The Neuronal Isoform of NO Synthase -- 1.2.3.1 Transcriptional Complexity and Splice Variants of nNOS -- 1.2.3.2 Regulation of nNOS Activity by Interaction with Other Proteins via its PDZ Domain -- 1.2.3.3 Regulation of nNOS Activity by Other Protein--Protein Interactions -- 1.2.3.4 Regulation of nNOS Activity by Phosphorylation -- 1.2.4 The Inducible Isoform of NO Synthase -- 1.2.4.1 Regulation of iNOS Activity by Protein--Protein Interactions -- 1.2.4.2 Regulation of iNOS Activity by Phosphorylation -- 1.2.5 The Endothelial Isoform of NO Synthase -- 1.2.5.1 Regulation of eNOS Activity by Protein--Protein Interaction -- 1.2.5.2 Regulation of eNOS Activity by Phosphorylation -- 1.3…Physiologic Functions of NO Produced by the Different Isoforms of NOS -- 1.3.1 Functions of nNOS in Physiology -- 1.3.1.1 Neuromodulation in the CNS -- 1.3.1.2 Atypical Neurotransmission in the Peripheral Nervous System -- 1.3.1.3 Importance of nNOS-Derived NO for Penile Erection---The Basis for the Action of Phosphodiesterase 5 Inhibitors -- 1.3.2 Functions of iNOS in Physiology -- 1.3.3 Functions of eNOS in Physiology -- 1.3.3.1 Vasodilation and Inhibition of Platelet Aggregation and Adhesion -- 1.3.3.2 Inhibition of Leukocyte Chemotaxis, Adhesion and Vascular Inflammation -- 1.3.3.3 Control of Vascular Smooth Muscle Proliferation -- 1.3.3.4 Stimulation of Angiogenesis by NO Derived Form eNOS -- 1.3.3.5 Activation of Endothelial Progenitor Cells by eNOS-Derived NO -- 1.4…Pathophysiologic Roles of NO Produced by the Different Isoforms of NOS.
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1.4.1 The Roles of nNOS in Pathophysiology -- 1.4.2 The Role of iNOS in Pathophysiology -- 1.4.3 Vascular Oxidative Stress and the Role of eNOS in Pathophysiology -- 1.4.4 Activation of the Renin--Angiotensin System Increases Oxidative Stress -- 1.4.5 A Reduced eNOS Expression is Unlikely to Contribute to Endothelial Dysfunction -- 1.4.6 Inactivation of NO and eNOS Uncoupling---The Molecular Bases for a Lack of Bioactive NO in Vascular Disease -- 1.4.6.1 The (6R-)5,6,7,8-tetrahydrobiopterin (BH4) Hypothesis -- 1.4.6.2 L-arginine Supply to eNOS and eNOS Uncoupling -- 1.4.6.3 Asymmetrical Dimethyl-L-arginine and eNOS Uncoupling -- 1.4.6.4 eNOS Uncoupling by S-Glutathionylation of the Enzyme -- 1.5…Gene Therapy with NOS -- 1.6…Conclusions -- Acknowledgments -- References -- 2 The Role of Carbon Monoxide as a Gasotransmitter in Cardiovascular and Metabolic Regulation -- Abstract -- 2.1…Introduction -- 2.2…How the Concept of ''Gasotransmitter'' Evolved -- 2.3…Classification of a Gasotransmitter -- 2.3.1 CO as a Gasotransmitter -- 2.4…Production of CO in the Cardiovascular System -- 2.5…Physiological Functions of CO in the Cardiovasculature -- 2.5.1 CO-Mediated Vasorelaxation -- 2.5.2 CO Effects on Cell Proliferation and Apoptosis -- 2.5.2.1 Anti-Apoptotic Effects of CO -- 2.5.2.2 Pro-Apoptotic Effects of CO -- 2.5.3 CO-Mediated Anti-Aggregatory Effects -- 2.5.4 CO-Related Angiogenesis -- 2.5.5 Anti-Inflammatory Effects of CO -- 2.5.6 Cardiac Protection from Tissue Reperfusion Injury -- 2.6…Pathophysiological Changes of CO Functions and Metabolism -- 2.6.1 Diabetes -- 2.6.2 Vascular Proliferative Diseases -- 2.6.2.1 Hypertension -- 2.6.2.2 Atherosclerosis -- 2.6.3 Myocardial Infarction -- 2.7…The Cellular and Molecular Mechanisms of CO Effects -- 2.7.1 CO-Induced ROS Production -- 2.7.2 Ion Channel Signaling -- 2.7.2.1 BKCa.
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2.7.2.2 Ca2+ Channel (L-Type) Receptors -- 2.7.2.3 Ligand-Gated P2X Receptors -- 2.7.2.4 ENaC -- 2.7.3 CO-Induced Activation of Major Signaling Pathways -- 2.7.3.1 MAPK -- 2.7.3.2 PI3K-Akt -- 2.7.3.3 STAT -- 2.7.3.4 PPAR -- 2.7.3.5 HIF-1 alpha -- 2.7.3.6 sGC -- 2.8…The Interaction of CO with NO and H2S -- 2.9…Perspectives -- Acknowledgments -- References -- 3 Physiological and Pathophysiological Functions of Hydrogen Sulfide -- Abstract -- 3.1…Introduction -- 3.2…Solubility and Membrane Permeability of H2S -- 3.3…Endogenous H2S Levels -- 3.3.1 Acid-Labile Sulfur -- 3.3.2 Bound Sulfane Sulfur -- 3.3.3 Free H2S -- 3.4…H2S-Sensitive Fluorescent Probes -- 3.4.1 SF1, SF2, and DNS-Az -- 3.4.2 Probe 1, SFP-1, and SFP-2 -- 3.4.3 HSIP-1 -- 3.5…H2S-Producing Enzymes -- 3.5.1 CBS -- 3.5.2 CSE -- 3.5.3 3MST and CAT -- 3.6…Physiological Functions of H2S -- 3.6.1 Signaling Functions of H2S -- 3.6.1.1 Synaptic Modulation in the Brain -- 3.6.1.2 Ca2+ Regulation in the Retina -- 3.6.1.3 Oxygen Sensor -- 3.6.1.4 Smooth Muscle Relaxation -- 3.6.2 Cytoprotective Functions of H2S -- 3.6.2.1 Increases in Glutathione Levels -- 3.6.2.2 ROS Scavenger -- 3.6.2.3 Inhibition of Apoptosis -- 3.6.2.4 Regulation of ER Stress -- 3.6.2.5 Regulation of Intracellular Ca2+ -- 3.6.2.6 Stabilizing the Membrane Potential -- 3.7…Pathophysiological Functions of H2S -- 3.7.1 Ethylmalonic Encephalopathy -- 3.7.2 Down's Syndrome -- 3.7.3 Renovascular Hypertension -- 3.7.4 Vascular Endothelial Dysfunction -- 3.7.5 Microcirculation in the Brain -- 3.8…Therapeutic Applications -- 3.9…Concluding Remarks -- Acknowledgements -- References -- 4 Methods for the Detection of Gasotransmitters -- Abstract -- 4.1…Introduction -- 4.2…Detection Methods of Nitric Oxide -- 4.2.1 Small Molecule Chemoprobes -- 4.2.2 Transition Metal-Based Probes for NO.
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4.2.3 Capillary Electrophoresis with Laser-Induced Fluorescence Detection -- 4.2.4 NO-Selective Electrodes -- 4.2.5 Protein-Based Probes for NO -- 4.3…Detection Methods of Hydrogen Sulfide -- 4.3.1 Chromatographic Methods -- 4.3.2 Reaction-Based Spectrophotometric Methods -- 4.3.2.1 Fluorescent Probes Based on Nucleophilic Addition/Substitution -- 4.3.2.2 Fluorescent Probes Based on Azide Reduction -- 4.3.2.3 Fluorescent Probes Based on Metal Sulfide Formation -- 4.3.3 Electrochemical Methods -- 4.4…Detection Methods of Carbon Monoxide -- 4.4.1 Spectrophotometric Methods -- 4.4.1.1 Spectrophotometric Methods Based on COHb Absorption -- 4.4.1.2 Derivative Absorption Spectrophotometric Methods -- 4.4.1.3 Reaction-Based Colorimetric Method -- 4.4.2 Gas Chromatographic Methods -- 4.4.3 Electrochemical Methods -- 4.5…Conclusions -- Acknowledgments -- References -- 5 Gasotransmitters in Regulation of Neuromuscular Transmission -- Abstract -- 5.1…Introduction -- 5.2…Nitric Oxide -- 5.3…Carbon Monoxide -- 5.4…Hydrogen Sulfide -- Acknowledgments -- References -- 6 Modulated by Gasotransmitters: BK Channels -- Abstract -- 6.1…Ion Channels -- 6.2…Calcium-Activated Potassium Channels -- 6.3…BK Channels -- 6.3.1 BK Channels: Structure and Function -- 6.3.2 BK Channel: Pharmacology -- 6.3.3 BK Channel Subunits -- 6.3.4 Posttranslational Modifications at BK Channels -- 6.3.5 BK Channelopathies -- 6.4…Gasotransmitters: BK Channels -- 6.5…BK Channels: Modulation by Nitric Oxide (NO) -- 6.5.1 NO--BK: Hormones -- 6.5.2 NO--BK Disorders -- 6.6…BK Channels: Modulation by Carbon Monoxide (CO) -- 6.7…BK Channels: Modulation by Hydrogen Sulfide (H2S) -- 6.7.1 BK Channels and Oxygen -- 6.8…Synopsis -- Acknowledgments -- References -- Index.
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