Coronary flow regulation in mouse heart during hypercapnic acidosis: Role of NO and its compensation during eNOS impairment

Cardiovascular Research

Volumn 77, Issue 1, 2008, Pages 188-196

  Heintz, Anke ^a   Damm, Martin ^a   Brand, Markus ^b   Koch, Thea ^a   Deussen, Andreas ^b  

^a UNIVERSITY HOSPITAL CARL GUSTAV CARUS   (Germany)

^b DRESDEN UNIVERSITY OF TECHNOLOGY   (Germany)

Author keywords

Acidosis; Coronary circulation; Hypercapnia; Nitric oxide; Potassium channels

Indexed keywords

1 (2 TRIFLUOROMETHYLPHENYL)IMIDAZOLE; 5 AMINO 2 (2 FURYL) 7 (2 PHENYLETHYL)PYRAZOLO[4,3 E][1,2,4]TRIAZOLO[1,5 C]PYRIMIDINE; ADENOSINE A2A RECEPTOR; ADENOSINE TRIPHOSPHATASE (POTASSIUM); CALCIUM ACTIVATED POTASSIUM CHANNEL; ENDOTHELIAL NITRIC OXIDE SYNTHASE; EPOXYICOSATRIENOIC ACID; GLIBENCLAMIDE; INDOMETACIN; MICONAZOLE; N(G) NITROARGININE METHYL ESTER; NITRIC OXIDE; PROSTAGLANDIN SYNTHASE; VOLTAGE GATED POTASSIUM CHANNEL;

ACIDOSIS; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTERIAL CARBON DIOXIDE TENSION; ARTICLE; CORONARY ARTERY BLOOD FLOW; ENZYME ACTIVATION; HEART MUSCLE OXYGEN CONSUMPTION; HEART PERFUSION; HYPERCAPNIA; KNOCKOUT MOUSE; MOUSE; NONHUMAN; PRIORITY JOURNAL; WILD TYPE;

ACIDOSIS; ANIMALS; CORONARY CIRCULATION; HYPERCAPNIA; KATP CHANNELS; MALE; MICE; MICE, INBRED C57BL; NG-NITROARGININE METHYL ESTER; NITRIC OXIDE; NITRIC OXIDE SYNTHASE TYPE III; POTASSIUM CHANNELS, CALCIUM-ACTIVATED; RECEPTORS, ADENOSINE A2;

EID: 38849085923     PISSN: 00086363     EISSN: 17553245     Source Type: Journal    
DOI: 10.1093/cvr/cvm014     Document Type: Article

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