| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 School of Sport and Exercise Sciences, University of Birmingham, Birmingham, United Kingdom; Department of Physiology, University of Birmingham, Birmingham, United Kingdom
2 Department of Physiology, University of Birmingham, Birmingham, United Kingdom
3 School of Sport and Exercise Sciences, University of Birmingham, Birmingham, United Kingdom
* To whom correspondence should be addressed. E-mail: O.hudlicka{at}bham.ac.uk.
Vascular endothelial growth factor (VEGF) is considered to be important in promotion of capillary growth in skeletal muscles exposed to increased activity. We studied its interactions with nitric oxide (NO) by examining the expression of eNOS, VEGF and VEGF receptor-2 proteins in relation to capillary growth in rat extensor digitorum longus muscles electrically stimulated for two, four or seven days with and without NO synthase inhibition by N
-nitro-l-arginine (L-NNA, 3 mg.day-1). Stimulation increased all proteins from two days onwards, concomitantly with capillary proliferation (labelling for proliferating cell nuclear antigen). Capillary:fiber ratio (C:F) was elevated by 25 % after seven days. Concurrent administration of oral L-NNA did not affect the increase in eNOS but depressed its activity, as shown by increased blood pressure and decreased arteriolar diameters in two day stimulated muscles. NOS inhibition eliminated the increased expression of VEGFR-2 and VEGF proteins in muscles stimulated for two and four days but not seven days. However, it depressed capillary proliferation and the increase in C:F ratio at all time points studied. We conclude that in stimulated muscles, NO, generated by activation of nNOS via muscle activity or eNOS by increased blood flow and capillary shear stress, may increase capillary proliferation in the early stages of stimulation through up-regulation of VEGFR-2 and VEGF. With longer stimulation, capillary growth appears to require NO, and high levels of VEGF and VEGFR-2 may be contributing to maintenance of the increased capillary bed.
This article has been cited by other articles:
|
|
 |
|
  T. Gustafsson, H. Rundqvist, J. Norrbom, E. Rullman, E. Jansson, and C. J. Sundberg The influence of physical training on the angiopoietin and VEGF-A systems in human skeletal muscle J Appl Physiol, September 1, 2007; 103(3): 1012 - 1020. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Mac Gabhann, J. W. Ji, and A. S. Popel VEGF gradients, receptor activation, and sprout guidance in resting and exercising skeletal muscle J Appl Physiol, February 1, 2007; 102(2): 722 - 734. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Milkiewicz, O. Hudlicka, R. Shiner, S. Egginton, and M. D. Brown Vascular endothelial growth factor mRNA and protein do not change in parallel during non-inflammatory skeletal muscle ischaemia in rat J. Physiol., December 1, 2006; 577(2): 671 - 678. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. Bhandari, R. Choo-Wing, S. P. Chapoval, C. G. Lee, C. Tang, Y. K. Kim, B. Ma, P. Baluk, M. I. Lin, D. M. McDonald, et al. Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung PNAS, July 18, 2006; 103(29): 11021 - 11026. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. J. Prior, J. M. Hagberg, C. M. Paton, L. W. Douglass, M. D. Brown, J. C. McLenithan, and S. M. Roth DNA sequence variation in the promoter region of the VEGF gene impacts VEGF gene expression and maximal oxygen consumption Am J Physiol Heart Circ Physiol, May 1, 2006; 290(5): H1848 - H1855. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Suzuki Microvascular angioadaptation after endurance training with L-arginine supplementation in rat heart and hindleg muscles Exp Physiol, September 1, 2005; 90(5): 763 - 771. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
