GlutaredoxinV1, Main, Exploration, bibRecord, 000398

β3 Adrenergic Stimulation Restores Nitric Oxide/Redox Balance and Enhances Endothelial Function in Hyperglycemia.

Identifieur interne : 000398 ( Main/Exploration ); précédent : 000397; suivant : 000399

β3 Adrenergic Stimulation Restores Nitric Oxide/Redox Balance and Enhances Endothelial Function in Hyperglycemia.

Auteurs : Keyvan Karimi Galougahi [États-Unis] ; Chia-Chi Liu [Australie] ; Alvaro Garcia [Australie] ; Carmine Gentile [Australie] ; Natasha A. Fry [Australie] ; Elisha J. Hamilton [Australie] ; Clare L. Hawkins [Australie] ; Gemma A. Figtree [Australie]

Source :

Journal of the American Heart Association [ 2047-9980 ] ; 2016.

RBID : pubmed:26896479

Descripteurs français

English descriptors

KwdEn :
- Adrenergic beta-3 Receptor Agonists (pharmacology), Animals (MeSH), Blood Glucose (drug effects), Blood Glucose (metabolism), Diabetes Mellitus, Experimental (chemically induced), Diabetes Mellitus, Experimental (drug therapy), Diabetes Mellitus, Experimental (enzymology), Diabetes Mellitus, Experimental (physiopathology), Diabetic Angiopathies (chemically induced), Diabetic Angiopathies (enzymology), Diabetic Angiopathies (physiopathology), Diabetic Angiopathies (prevention & control), Dioxoles (pharmacology), Dose-Response Relationship, Drug (MeSH), Endothelium, Vascular (drug effects), Endothelium, Vascular (enzymology), Endothelium, Vascular (physiopathology), Enzyme Activation (MeSH), Glutathione (metabolism), Hyperglycemia (chemically induced), Hyperglycemia (drug therapy), Hyperglycemia (enzymology), Hyperglycemia (physiopathology), Hypoglycemic Agents (pharmacology), Male (MeSH), NADPH Oxidases (metabolism), Nitric Oxide (metabolism), Nitric Oxide Synthase Type III (metabolism), Oxidation-Reduction (MeSH), Oxidative Stress (drug effects), Peptides (MeSH), Rabbits (MeSH), Receptors, Adrenergic, beta-3 (drug effects), Receptors, Adrenergic, beta-3 (metabolism), Signal Transduction (drug effects), Sodium-Potassium-Exchanging ATPase (metabolism), Superoxides (metabolism), Time Factors (MeSH).
MESH :
- chemical , drug effects : Blood Glucose, Receptors, Adrenergic, beta-3.
- chemical , metabolism : Blood Glucose, Glutathione, NADPH Oxidases, Nitric Oxide, Nitric Oxide Synthase Type III, Receptors, Adrenergic, beta-3, Sodium-Potassium-Exchanging ATPase, Superoxides.
- chemical , pharmacology : Adrenergic beta-3 Receptor Agonists, Dioxoles, Hypoglycemic Agents.
- chemically induced : Diabetes Mellitus, Experimental, Diabetic Angiopathies, Hyperglycemia.
- drug effects : Endothelium, Vascular, Oxidative Stress, Signal Transduction.
- drug therapy : Diabetes Mellitus, Experimental, Hyperglycemia.
- enzymology : Diabetes Mellitus, Experimental, Diabetic Angiopathies, Endothelium, Vascular, Hyperglycemia.
- physiopathology : Diabetes Mellitus, Experimental, Diabetic Angiopathies, Endothelium, Vascular, Hyperglycemia.
- prevention & control : Diabetic Angiopathies.
- Animals, Dose-Response Relationship, Drug, Enzyme Activation, Male, Oxidation-Reduction, Peptides, Rabbits, Time Factors.

Abstract

BACKGROUND

Perturbed balance between NO and O2 (•-). (ie, NO/redox imbalance) is central in the pathobiology of diabetes-induced vascular dysfunction. We examined whether stimulation of β3 adrenergic receptors (β3 ARs), coupled to endothelial nitric oxide synthase (eNOS) activation, would re-establish NO/redox balance, relieve oxidative inhibition of the membrane proteins eNOS and Na(+)-K(+) (NK) pump, and improve vascular function in a new animal model of hyperglycemia.

METHODS AND RESULTS

We established hyperglycemia in male White New Zealand rabbits by infusion of S961, a competitive high-affinity peptide inhibitor of the insulin receptor. Hyperglycemia impaired endothelium-dependent vasorelaxation by "uncoupling" of eNOS via glutathionylation (eNOS-GSS) that was dependent on NADPH oxidase activity. Accordingly, NO levels were lower while O2 (•-) levels were higher in hyperglycemic rabbits. Infusion of the β3 AR agonist CL316243 (CL) decreased eNOS-GSS, reduced O2 (•-), restored NO levels, and improved endothelium-dependent relaxation. CL decreased hyperglycemia-induced NADPH oxidase activation as suggested by co-immunoprecipitation experiments, and it increased eNOS co-immunoprecipitation with glutaredoxin-1, which may reflect promotion of eNOS de-glutathionylation by CL. Moreover, CL reversed hyperglycemia-induced glutathionylation of the β1 NK pump subunit that causes NK pump inhibition, and improved K(+)-induced vasorelaxation that reflects enhancement in NK pump activity. Lastly, eNOS-GSS was higher in vessels of diabetic patients and was reduced by CL, suggesting potential significance of the experimental findings in human diabetes.

CONCLUSIONS

β3 AR activation restored NO/redox balance and improved endothelial function in hyperglycemia. β3 AR agonists may confer protection against diabetes-induced vascular dysfunction.

DOI: 10.1161/JAHA.115.002824
PubMed: 26896479
PubMed Central: PMC4802476

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000460
to stream Main, to step Curation: 000460

Le document en format XML

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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adrenergic beta-3 Receptor Agonists (pharmacology)</term>
<term>Animals (MeSH)</term>
<term>Blood Glucose (drug effects)</term>
<term>Blood Glucose (metabolism)</term>
<term>Diabetes Mellitus, Experimental (chemically induced)</term>
<term>Diabetes Mellitus, Experimental (drug therapy)</term>
<term>Diabetes Mellitus, Experimental (enzymology)</term>
<term>Diabetes Mellitus, Experimental (physiopathology)</term>
<term>Diabetic Angiopathies (chemically induced)</term>
<term>Diabetic Angiopathies (enzymology)</term>
<term>Diabetic Angiopathies (physiopathology)</term>
<term>Diabetic Angiopathies (prevention & control)</term>
<term>Dioxoles (pharmacology)</term>
<term>Dose-Response Relationship, Drug (MeSH)</term>
<term>Endothelium, Vascular (drug effects)</term>
<term>Endothelium, Vascular (enzymology)</term>
<term>Endothelium, Vascular (physiopathology)</term>
<term>Enzyme Activation (MeSH)</term>
<term>Glutathione (metabolism)</term>
<term>Hyperglycemia (chemically induced)</term>
<term>Hyperglycemia (drug therapy)</term>
<term>Hyperglycemia (enzymology)</term>
<term>Hyperglycemia (physiopathology)</term>
<term>Hypoglycemic Agents (pharmacology)</term>
<term>Male (MeSH)</term>
<term>NADPH Oxidases (metabolism)</term>
<term>Nitric Oxide (metabolism)</term>
<term>Nitric Oxide Synthase Type III (metabolism)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Oxidative Stress (drug effects)</term>
<term>Peptides (MeSH)</term>
<term>Rabbits (MeSH)</term>
<term>Receptors, Adrenergic, beta-3 (drug effects)</term>
<term>Receptors, Adrenergic, beta-3 (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
<term>Sodium-Potassium-Exchanging ATPase (metabolism)</term>
<term>Superoxides (metabolism)</term>
<term>Time Factors (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation enzymatique (MeSH)</term>
<term>Agonistes des récepteurs bêta-3 adrénergiques (pharmacologie)</term>
<term>Angiopathies diabétiques (enzymologie)</term>
<term>Angiopathies diabétiques (induit chimiquement)</term>
<term>Angiopathies diabétiques (physiopathologie)</term>
<term>Angiopathies diabétiques (prévention et contrôle)</term>
<term>Animaux (MeSH)</term>
<term>Diabète expérimental (enzymologie)</term>
<term>Diabète expérimental (induit chimiquement)</term>
<term>Diabète expérimental (physiopathologie)</term>
<term>Diabète expérimental (traitement médicamenteux)</term>
<term>Dioxoles (pharmacologie)</term>
<term>Endothélium vasculaire (effets des médicaments et des substances chimiques)</term>
<term>Endothélium vasculaire (enzymologie)</term>
<term>Endothélium vasculaire (physiopathologie)</term>
<term>Facteurs temps (MeSH)</term>
<term>Glutathion (métabolisme)</term>
<term>Glycémie (effets des médicaments et des substances chimiques)</term>
<term>Glycémie (métabolisme)</term>
<term>Hyperglycémie (enzymologie)</term>
<term>Hyperglycémie (induit chimiquement)</term>
<term>Hyperglycémie (physiopathologie)</term>
<term>Hyperglycémie (traitement médicamenteux)</term>
<term>Hypoglycémiants (pharmacologie)</term>
<term>Lapins (MeSH)</term>
<term>Monoxyde d'azote (métabolisme)</term>
<term>Mâle (MeSH)</term>
<term>NADPH oxidase (métabolisme)</term>
<term>Nitric oxide synthase type III (métabolisme)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Peptides (MeSH)</term>
<term>Relation dose-effet des médicaments (MeSH)</term>
<term>Récepteurs bêta-3 adrénergiques (effets des médicaments et des substances chimiques)</term>
<term>Récepteurs bêta-3 adrénergiques (métabolisme)</term>
<term>Sodium-Potassium-Exchanging ATPase (métabolisme)</term>
<term>Stress oxydatif (effets des médicaments et des substances chimiques)</term>
<term>Superoxydes (métabolisme)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Blood Glucose</term>
<term>Receptors, Adrenergic, beta-3</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Blood Glucose</term>
<term>Glutathione</term>
<term>NADPH Oxidases</term>
<term>Nitric Oxide</term>
<term>Nitric Oxide Synthase Type III</term>
<term>Receptors, Adrenergic, beta-3</term>
<term>Sodium-Potassium-Exchanging ATPase</term>
<term>Superoxides</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adrenergic beta-3 Receptor Agonists</term>
<term>Dioxoles</term>
<term>Hypoglycemic Agents</term>
</keywords>
<keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Diabetes Mellitus, Experimental</term>
<term>Diabetic Angiopathies</term>
<term>Hyperglycemia</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Endothelium, Vascular</term>
<term>Oxidative Stress</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Diabetes Mellitus, Experimental</term>
<term>Hyperglycemia</term>
</keywords>
<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Endothélium vasculaire</term>
<term>Glycémie</term>
<term>Récepteurs bêta-3 adrénergiques</term>
<term>Stress oxydatif</term>
<term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Angiopathies diabétiques</term>
<term>Diabète expérimental</term>
<term>Endothélium vasculaire</term>
<term>Hyperglycémie</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Diabetes Mellitus, Experimental</term>
<term>Diabetic Angiopathies</term>
<term>Endothelium, Vascular</term>
<term>Hyperglycemia</term>
</keywords>
<keywords scheme="MESH" qualifier="induit chimiquement" xml:lang="fr"><term>Angiopathies diabétiques</term>
<term>Diabète expérimental</term>
<term>Hyperglycémie</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Glutathion</term>
<term>Glycémie</term>
<term>Monoxyde d'azote</term>
<term>NADPH oxidase</term>
<term>Nitric oxide synthase type III</term>
<term>Récepteurs bêta-3 adrénergiques</term>
<term>Sodium-Potassium-Exchanging ATPase</term>
<term>Superoxydes</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Agonistes des récepteurs bêta-3 adrénergiques</term>
<term>Dioxoles</term>
<term>Hypoglycémiants</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Angiopathies diabétiques</term>
<term>Diabète expérimental</term>
<term>Endothélium vasculaire</term>
<term>Hyperglycémie</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Diabetes Mellitus, Experimental</term>
<term>Diabetic Angiopathies</term>
<term>Endothelium, Vascular</term>
<term>Hyperglycemia</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Diabetic Angiopathies</term>
</keywords>
<keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Angiopathies diabétiques</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Diabète expérimental</term>
<term>Hyperglycémie</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Dose-Response Relationship, Drug</term>
<term>Enzyme Activation</term>
<term>Male</term>
<term>Oxidation-Reduction</term>
<term>Peptides</term>
<term>Rabbits</term>
<term>Time Factors</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation enzymatique</term>
<term>Animaux</term>
<term>Facteurs temps</term>
<term>Lapins</term>
<term>Mâle</term>
<term>Oxydoréduction</term>
<term>Peptides</term>
<term>Relation dose-effet des médicaments</term>
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<front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b>
</p>
<p>Perturbed balance between NO and O2 (•-). (ie, NO/redox imbalance) is central in the pathobiology of diabetes-induced vascular dysfunction. We examined whether stimulation of β3 adrenergic receptors (β3 ARs), coupled to endothelial nitric oxide synthase (eNOS) activation, would re-establish NO/redox balance, relieve oxidative inhibition of the membrane proteins eNOS and Na(+)-K(+) (NK) pump, and improve vascular function in a new animal model of hyperglycemia.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>METHODS AND RESULTS</b>
</p>
<p>We established hyperglycemia in male White New Zealand rabbits by infusion of S961, a competitive high-affinity peptide inhibitor of the insulin receptor. Hyperglycemia impaired endothelium-dependent vasorelaxation by "uncoupling" of eNOS via glutathionylation (eNOS-GSS) that was dependent on NADPH oxidase activity. Accordingly, NO levels were lower while O2 (•-) levels were higher in hyperglycemic rabbits. Infusion of the β3 AR agonist CL316243 (CL) decreased eNOS-GSS, reduced O2 (•-), restored NO levels, and improved endothelium-dependent relaxation. CL decreased hyperglycemia-induced NADPH oxidase activation as suggested by co-immunoprecipitation experiments, and it increased eNOS co-immunoprecipitation with glutaredoxin-1, which may reflect promotion of eNOS de-glutathionylation by CL. Moreover, CL reversed hyperglycemia-induced glutathionylation of the β1 NK pump subunit that causes NK pump inhibition, and improved K(+)-induced vasorelaxation that reflects enhancement in NK pump activity. Lastly, eNOS-GSS was higher in vessels of diabetic patients and was reduced by CL, suggesting potential significance of the experimental findings in human diabetes.</p>
</div>
<div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b>
</p>
<p>β3 AR activation restored NO/redox balance and improved endothelial function in hyperglycemia. β3 AR agonists may confer protection against diabetes-induced vascular dysfunction.</p>
</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26896479</PMID>
<DateCompleted><Year>2017</Year>
<Month>01</Month>
<Day>10</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">2047-9980</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>5</Volume>
<Issue>2</Issue>
<PubDate><Year>2016</Year>
<Month>Feb</Month>
<Day>19</Day>
</PubDate>
</JournalIssue>
<Title>Journal of the American Heart Association</Title>
<ISOAbbreviation>J Am Heart Assoc</ISOAbbreviation>
</Journal>
<ArticleTitle>β3 Adrenergic Stimulation Restores Nitric Oxide/Redox Balance and Enhances Endothelial Function in Hyperglycemia.</ArticleTitle>
<ELocationID EIdType="doi" ValidYN="Y">10.1161/JAHA.115.002824</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">e002824</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Perturbed balance between NO and O2 (•-). (ie, NO/redox imbalance) is central in the pathobiology of diabetes-induced vascular dysfunction. We examined whether stimulation of β3 adrenergic receptors (β3 ARs), coupled to endothelial nitric oxide synthase (eNOS) activation, would re-establish NO/redox balance, relieve oxidative inhibition of the membrane proteins eNOS and Na(+)-K(+) (NK) pump, and improve vascular function in a new animal model of hyperglycemia.</AbstractText>
<AbstractText Label="METHODS AND RESULTS" NlmCategory="RESULTS">We established hyperglycemia in male White New Zealand rabbits by infusion of S961, a competitive high-affinity peptide inhibitor of the insulin receptor. Hyperglycemia impaired endothelium-dependent vasorelaxation by "uncoupling" of eNOS via glutathionylation (eNOS-GSS) that was dependent on NADPH oxidase activity. Accordingly, NO levels were lower while O2 (•-) levels were higher in hyperglycemic rabbits. Infusion of the β3 AR agonist CL316243 (CL) decreased eNOS-GSS, reduced O2 (•-), restored NO levels, and improved endothelium-dependent relaxation. CL decreased hyperglycemia-induced NADPH oxidase activation as suggested by co-immunoprecipitation experiments, and it increased eNOS co-immunoprecipitation with glutaredoxin-1, which may reflect promotion of eNOS de-glutathionylation by CL. Moreover, CL reversed hyperglycemia-induced glutathionylation of the β1 NK pump subunit that causes NK pump inhibition, and improved K(+)-induced vasorelaxation that reflects enhancement in NK pump activity. Lastly, eNOS-GSS was higher in vessels of diabetic patients and was reduced by CL, suggesting potential significance of the experimental findings in human diabetes.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">β3 AR activation restored NO/redox balance and improved endothelial function in hyperglycemia. β3 AR agonists may confer protection against diabetes-induced vascular dysfunction.</AbstractText>
<CopyrightInformation>© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Karimi Galougahi</LastName>
<ForeName>Keyvan</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>North Shore Heart Research Group, Kolling Institute, University of Sydney, Australia University of Sydney Medical School Foundation, Sydney, Australia Columbia University Medical Center, New York, NY.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Chia-Chi</ForeName>
<Initials>CC</Initials>
<AffiliationInfo><Affiliation>North Shore Heart Research Group, Kolling Institute, University of Sydney, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Garcia</LastName>
<ForeName>Alvaro</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>North Shore Heart Research Group, Kolling Institute, University of Sydney, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gentile</LastName>
<ForeName>Carmine</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>School of Medicine, University of Sydney, Australia Heart Research Institute, Sydney, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Fry</LastName>
<ForeName>Natasha A</ForeName>
<Initials>NA</Initials>
<AffiliationInfo><Affiliation>North Shore Heart Research Group, Kolling Institute, University of Sydney, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hamilton</LastName>
<ForeName>Elisha J</ForeName>
<Initials>EJ</Initials>
<AffiliationInfo><Affiliation>North Shore Heart Research Group, Kolling Institute, University of Sydney, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hawkins</LastName>
<ForeName>Clare L</ForeName>
<Initials>CL</Initials>
<AffiliationInfo><Affiliation>Heart Research Institute, Sydney, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Figtree</LastName>
<ForeName>Gemma A</ForeName>
<Initials>GA</Initials>
<AffiliationInfo><Affiliation>North Shore Heart Research Group, Kolling Institute, University of Sydney, Australia Department of Cardiology, Royal North Shore Hospital, Sydney, Australia gemma.figtree@sydney.edu.au.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>02</Month>
<Day>19</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Am Heart Assoc</MedlineTA>
<NlmUniqueID>101580524</NlmUniqueID>
<ISSNLinking>2047-9980</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D058667">Adrenergic beta-3 Receptor Agonists</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D001786">Blood Glucose</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004149">Dioxoles</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D007004">Hypoglycemic Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D010455">Peptides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D022702">Receptors, Adrenergic, beta-3</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C532752">S961 peptide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>11062-77-4</RegistryNumber>
<NameOfSubstance UI="D013481">Superoxides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>138908-40-4</RegistryNumber>
<NameOfSubstance UI="C076126">disodium (R,R)-5-(2-((2-(3-chlorophenyl)-2-hydroxyethyl)-amino)propyl)-1,3-benzodioxole-2,3-dicarboxylate</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>31C4KY9ESH</RegistryNumber>
<NameOfSubstance UI="D009569">Nitric Oxide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.14.13.39</RegistryNumber>
<NameOfSubstance UI="D052250">Nitric Oxide Synthase Type III</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 1.6.3.-</RegistryNumber>
<NameOfSubstance UI="D019255">NADPH Oxidases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 7.2.2.13</RegistryNumber>
<NameOfSubstance UI="D000254">Sodium-Potassium-Exchanging ATPase</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber>
<NameOfSubstance UI="D005978">Glutathione</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D058667" MajorTopicYN="N">Adrenergic beta-3 Receptor Agonists</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001786" MajorTopicYN="N">Blood Glucose</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003921" MajorTopicYN="N">Diabetes Mellitus, Experimental</DescriptorName>
<QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003925" MajorTopicYN="N">Diabetic Angiopathies</DescriptorName>
<QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName>
<QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
<QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004149" MajorTopicYN="N">Dioxoles</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004305" MajorTopicYN="N">Dose-Response Relationship, Drug</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004730" MajorTopicYN="N">Endothelium, Vascular</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004789" MajorTopicYN="N">Enzyme Activation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006943" MajorTopicYN="N">Hyperglycemia</DescriptorName>
<QualifierName UI="Q000139" MajorTopicYN="N">chemically induced</QualifierName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName>
<QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007004" MajorTopicYN="N">Hypoglycemic Agents</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019255" MajorTopicYN="N">NADPH Oxidases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009569" MajorTopicYN="N">Nitric Oxide</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D052250" MajorTopicYN="N">Nitric Oxide Synthase Type III</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010084" MajorTopicYN="N">Oxidation-Reduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010455" MajorTopicYN="N">Peptides</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011817" MajorTopicYN="N">Rabbits</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D022702" MajorTopicYN="N">Receptors, Adrenergic, beta-3</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000254" MajorTopicYN="N">Sodium-Potassium-Exchanging ATPase</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013481" MajorTopicYN="N">Superoxides</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">endothelial dysfunction</Keyword>
<Keyword MajorTopicYN="N">endothelial nitric oxide synthase</Keyword>
<Keyword MajorTopicYN="N">hyperglycemia</Keyword>
<Keyword MajorTopicYN="N">oxidative stress</Keyword>
<Keyword MajorTopicYN="N">β3 adrenergic receptors</Keyword>
</KeywordList>
</MedlineCitation>
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β3 Adrenergic Stimulation Restores Nitric Oxide/Redox Balance and Enhances Endothelial Function in Hyperglycemia.

β3 Adrenergic Stimulation Restores Nitric Oxide/Redox Balance and Enhances Endothelial Function in Hyperglycemia.

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