β3-adrenoceptor, glutathionylation, and diabetic cardiomyopathy. Focus on “β3-adrenoceptor activation relieves oxidative inhibition of the cardiac Na+-K+ pump in hyperglycemia induced by insulin receptor blockade”

American Journal of Physiology - Cell Physiology

Volumn 309, Issue 5, 2015, Pages C283-C285

  Black, Stephen M ^a  

^a UNIVERSITY OF ARIZONA COLLEGE OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

BETA 3 ADRENERGIC RECEPTOR; GLUTATHIONE; INSULIN RECEPTOR; NITRIC OXIDE; ADENOSINE TRIPHOSPHATASE (POTASSIUM SODIUM); BETA ADRENERGIC RECEPTOR STIMULATING AGENT;

CELL METABOLISM; DIABETIC CARDIOMYOPATHY; EDITORIAL; HEART MUSCLE; HEART VENTRICLE FUNCTION; HUMAN; HYPERGLYCEMIA; OXIDATIVE STRESS; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN GLUTATHIONYLATION; PROTEIN MODIFICATION; RENIN ANGIOTENSIN ALDOSTERONE SYSTEM; UPREGULATION; ANIMAL; ANTAGONISTS AND INHIBITORS; DIABETIC CARDIOMYOPATHIES; DRUG DELIVERY SYSTEM; DRUG EFFECTS; METABOLISM; PHYSIOLOGY; TRENDS;

ADRENERGIC BETA-AGONISTS; ANIMALS; DIABETIC CARDIOMYOPATHIES; DRUG DELIVERY SYSTEMS; GLUTATHIONE; HUMANS; HYPERGLYCEMIA; OXIDATIVE STRESS; RECEPTOR, INSULIN; RECEPTORS, ADRENERGIC, BETA-3; SODIUM-POTASSIUM-EXCHANGING ATPASE;

EID: 84940742651     PISSN: 03636143     EISSN: 15221563     Source Type: Journal    
DOI: 10.1152/ajpcell.00196.2015     Document Type: Editorial

References (10)

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