| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Department of Pharmacology, Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, Connecticut 06536-0812; 2 Department of Physiology, New York Medical College, Valhalla, New York 10595; and 3 Vascular Biology Center and Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta, Georgia 30912-2500
The goal of the present study was to develop a competitive PCR assay to measure changes in the expression of endothelial nitric oxide synthase (eNOS) mRNA levels throughout the canine vascular tree. A partial sequence of canine eNOS cDNA (1.86 kb), inducible NOS (1.95 kb), and neuronal NOS (1.16 kb) was cultured from canine aortic endothelial cells, LPS-treated canine splenic vein endothelial cells, and from canine left ventricle, respectively. Competitor eNOS cDNA (eNOS-C) was constructed via recombinant PCR. Thus, with the use of a standard curve competitive PCR with eNOS-C, the amount of eNOS mRNA in 500 ng of total RNA was greatest in the circumflex > right coronary artery > left anterior descending coronary artery > aorta. The isolation of coronary microvessels from the left ventricle was associated with an enrichment of endothelial cell markers such as eNOS, von Willebrand factor, and caveolin-1, an observation supported by the detection of up to 15-fold higher levels of eNOS mRNA in coronary microvessels relative to the larger arteries. The ability to quantify changes in eNOS mRNA levels throughout the canine vasculature should provide greater insight into the molecular mechanisms of how this gene is regulated in physiological and pathophysiological states.
nitric oxide; nitric oxide synthase; microvessels; complimentary deoxyribonucleic acid; endothelium
This article has been cited by other articles:
|
|
 |
|
  J.-L. Balligand, O. Feron, and C. Dessy eNOS Activation by Physical Forces: From Short-Term Regulation of Contraction to Chronic Remodeling of Cardiovascular Tissues Physiol Rev, April 1, 2009; 89(2): 481 - 534. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. D. Rudic, D. Brinster, Y. Cheng, S. Fries, W.-L. Song, S. Austin, T. M. Coffman, and G. A. FitzGerald COX-2-Derived Prostacyclin Modulates Vascular Remodeling Circ. Res., June 24, 2005; 96(12): 1240 - 1247. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Funabiki, K. Onishi, K. Dohi, T. Koji, K. Imanaka-Yoshida, M. Ito, H. Wada, N. Isaka, T. Nobori, and T. Nakano Combined angiotensin receptor blocker and ACE inhibitor on myocardial fibrosis and left ventricular stiffness in dogs with heart failure Am J Physiol Heart Circ Physiol, December 1, 2004; 287(6): H2487 - H2492. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. L. Brutsaert Cardiac Endothelial-Myocardial Signaling: Its Role in Cardiac Growth, Contractile Performance, and Rhythmicity Physiol Rev, January 1, 2003; 83(1): 59 - 115. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Fujii, A. Wada, T. Tsutamoto, M. Ohnishi, T. Isono, and M. Kinoshita Bradykinin Improves Left Ventricular Diastolic Function Under Long-Term Angiotensin-Converting Enzyme Inhibition in Heart Failure Hypertension, May 1, 2002; 39(5): 952 - 957. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. D. Rudic, M. Bucci, D. Fulton, S. S. Segal, and W. C. Sessa Temporal Events Underlying Arterial Remodeling After Chronic Flow Reduction in Mice : Correlation of Structural Changes With a Deficit in Basal Nitric Oxide Synthesis Circ. Res., June 9, 2000; 86(11): 1160 - 1166. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
