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1 Physiology, New York Medical College, Valhalla, NY, USA
2 Cell Biology and Genetics, and Vascular Surgery, Erasmus University Medical Center, Rotterdam, The Netherlands; Cell Biology and Genetics, and Vascular Surgery, Erasmus University Medical Center, Rotterdam, The Netherlands
3 Molecular and Cellular Physiology, LSU Health Sciences Center, Shreveport, LA, USA
* To whom correspondence should be addressed. E-mail: Thomas_Hintze{at}nymc.edu.
Our objective was to investigate the potential role of selective eNOS overexpression in coronary blood vessels in the control of myocardial oxygen consumption. Transgenic eNOS overexpressing mice (eNOS Tg) (n=22) and wild-type (WT) mice (n=24) were studied. Western blotting indicated greater than 6 fold increase of eNOS in cardiac tissue. Echocardiography in awake mice indicated no difference in cardiac function between WT and eNOS Tg, however, MAP in eNOS Tg mice decreased significantly (SP 126±2.3 to 109±2.3, p<0.05), while HR was not different. TPR was also decreased (9.8±0.8 to 7.6±0.4, p<0.05) in eNOS Tg. Furthermore, female eNOS Tg mice showed even lower TPR (7.2±0.4 mmHg/ml/min) compared to male eNOS Tg mice (8.6±0.5, mmHg/ml/min p<0.05). Left ventricular slices were isolated from WT and eNOS Tg mice. Using a Clark-type oxygen electrode in an airtight bath, myocardial oxygen consumption (MVO2)was determined as a percent decrease during increasing doses (10-10 to 10-4 mol/L) of bradykinin (BK), carbachol (CCh), forskolin (10-12 to 10-6 mol/L), or SNAP (10-7to 10-4 mol/L). Baseline MVO2 was not different between WT (181±13 nmol/g/min) and eNOS Tg (188±14 nmol/g/min). BK decreased MVO2, (10-4 mol/L) in WT by 17%±1.1 and 33%±2.7 in eNOS Tg (p<0.05). CCh also decreased MVO2, (10-4 mol/L) in WT by 20%±1.7 and 31%±2.0 in eNOS Tg (p<0.05). Forskolin (10-6 mol/L) or SNAP (10-4 mol/L) also decreased MVO2 in WT by 24%±2.8, and 36%±1.8 vs. eNOS 31%±1.8, and 37%±3.5 respectively. L-NAME, 10-3 mol/L, inhibited the MVO2 reduction to BK, CCh, and to forskolin by a similar degree (p<0.05), but not to SNAP. Thus, selective overexpression of eNOS in cardiac blood vessels in mice enhances the control of myocardial oxygen consumption by eNOS derived NO.
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