| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1Department of Physiology, New York Medical College, Valhalla, New York 10595; 2Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana 71130-3932; and 3Department of Cell Biology and Genetics and 4Department of Vascular Surgery, Erasmus University Medical Center, Rotterdam 3000 DR, The Netherlands
Submitted 16 March 2004 ; accepted in final form 13 July 2004
Our objective was to investigate the potential role of selective endothelial nitric oxide (NO) synthase (eNOS) overexpression in coronary blood vessels in the control of myocardial oxygen consumption (MVO2). Transgenic (Tg) eNOS-overexpressing mice (eNOS Tg) (n = 22) and wild-type (WT) mice (n = 24) were studied. Western blot analysis indicated greater than sixfold increase of eNOS in cardiac tissue. Echocardiography in awake mice indicated no difference in cardiac function between WT and eNOS Tg; however, systolic pressure in eNOS Tg mice decreased significantly (126 ± 2.3 to 109 ± 2.3 mmHg; P < 0.05), whereas heart rate (HR) was not different. Total peripheral resistance (TPR) was also decreased (9.8 ± 0.8 to 7.6 ± 0.4 4 mmHg·ml–1·min; P < 0.05) in eNOS Tg. Furthermore, female eNOS Tg mice showed even lower TPR (7.2 ± 0.4 mmHg·ml–1·min) compared with male eNOS mice (8.6 ± 0.5, mmHg·ml·min–1; P < 0.05). Left ventricular slices were isolated from WT and eNOS Tg mice. With the use of a Clark-type oxygen electrode in an airtight bath, MVO2 was determined as the 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 S-nitroso-N-acetyl penicillamine (SNAP; 10–7 to 10–4 mol/l). Baseline MVO2 was not different between WT (181 ± 13 nmol·g–1·min–1) and eNOS Tg (188 ± 14 nmol·g–1·min–1). 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 versus eNOS 31% ± 1.8 and 37% ± 3.5, respectively. N-nitro-L-arginine methyl ester (10–3 mol/l) inhibited the MVO2 reduction to BK, CCh, and 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 MVO2 by eNOS-derived NO.
forskolin; nitric oxide
This article has been cited by other articles:
|
|
 |
|
  S. Matsuhisa, H. Otani, T. Okazaki, K. Yamashita, Y. Akita, D. Sato, A. Moriguchi, H. Imamura, and T. Iwasaka Angiotensin II type 1 receptor blocker preserves tolerance to ischemia-reperfusion injury in Dahl salt-sensitive rat heart Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2473 - H2479. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. G. Williams, T. Rincon-Skinner, D. Sun, Z. Wang, S. Zhang, X. Zhang, and T. H. Hintze Role of nitric oxide in the coupling of myocardial oxygen consumption and coronary vascular dynamics during pregnancy in the dog Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2479 - H2486. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. W. Elrod, J. J.M. Greer, N. S. Bryan, W. Langston, J. F. Szot, H. Gebregzlabher, S. Janssens, M. Feelisch, and D. J. Lefer Cardiomyocyte-Specific Overexpression of NO Synthase-3 Protects Against Myocardial Ischemia-Reperfusion Injury Arterioscler Thromb Vasc Biol, July 1, 2006; 26(7): 1517 - 1523. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Zhao, G. He, Y.-R. Chen, R. P. Pandian, P. Kuppusamy, and J. L. Zweier Endothelium-Derived Nitric Oxide Regulates Postischemic Myocardial Oxygenation and Oxygen Consumption by Modulation of Mitochondrial Electron Transport Circulation, June 7, 2005; 111(22): 2966 - 2972. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
