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Increased basal and adenosine‐mediated coronary flow in ex vivo hearts from type I diabetic mice (1051.16)
Author(s) -
Labazi Hicham,
Zhou Xueping,
Teng Bunyen,
Mustafa S. Jamal
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1051.16
Subject(s) - medicine , endocrinology , adenosine , streptozotocin , agonist , diabetes mellitus , cgs 21680 , basal (medicine) , heart rate , type 2 diabetes , chemistry , adenosine receptor , blood pressure , receptor
Diabetes is known to cause morphological and functional changes in the cardiovascular system, resulting in abnormal responses to various stimuli such as adenosine. Our aim was to examine the functional changes in coronary flow (CF) to adenosine receptor (AR) agonists resulting from type I diabetes. Diabetes was induced in mice using streptozotocin (STZ, 10mg/Kg; 8 weeks) and concentration response curves to the non‐selective AR agonist NECA and to the A 2A AR selective agonist (CGS‐21680; CGS) were performed in isolated perfused hearts from STZ and vehicle (C) group. Diabetes resulted in a decrease in heart weight (0.093g ± 0.002 in STZ vs. 0.117g ± 0.004 in C; p<0.05), an increase in blood glucose level (510.8mg/dL ± 22.2 in STZ vs. 140.9mg/dL ± 9.4 in C; p<0.05) and an increase in the basal coronary flow (21.6 ± 1.5 in STZ vs. 16.1 ± 0.6 in C; p<0.05). Both NECA and CGS induced a concentration‐dependent increase in CF (ml.min ‐1 .mg ‐1 ) which was significantly increased in STZ compared to C (NECA: E max 39.8 ± 1.8 in STZ vs. 28.2 ± 0.7 in C; p<0.05) (CGS; E max 38.8 ± 1 in STZ vs. 28.3 ± 1.8 in C; p<0.05). No significant differences were observed between the groups for changes in both heart rate and left ventricular diastolic pressure to both agonists. Our data suggest that STZ‐induced diabetes resulted in an increase in basal CF as well as increased vasodilatory response to adenosine agonists, probably by upregulating A 2A receptor signaling. Grant Funding Source : Supported by HL 094447 and HL 027339