| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Physiology, LSU Health Sciences Center, New Orleans, Louisiana, United States
* To whom correspondence should be addressed. E-mail: jtune{at}lsuhsc.edu.
Elevated plasma levels of fat-derived signaling molecules are associated with obesity, vascular endothelial dysfunction, and coronary heart disease; however, little is known about their direct coronary vascular effects. Accordingly, we examined mechanisms by which one adipokine, resistin, affects coronary vascular tone and endothelial function. Studies were conducted in anesthetized dogs and isolated coronary artery rings. Resistin did not change coronary blood flow, mean arterial pressure, or heart rate. Resistin had no effect on acetylcholine-induced relaxation of artery rings; however, resistin did impair bradykinin-induced relaxation. Selective impairment was also observed in vivo, as resistin attenuated vasodilation to bradykinin but not acetylcholine. Resistin had no effect on dihydroethidium fluorescence, an indicator of superoxide (O2-) production and the inhibitory effect of resistin on bradykinin-induced relaxation persisted in the presence of Tempol, a superoxide dismutase mimetic. To determine whether resistin impaired production of and/or responses to nitric oxide (NO) or prostaglandins (e.g., prostacyclin; PGI2), we performed experiments with N
-nitro-L-arginine methyl ester (L-NAME) and indomethacin in vivo and in vitro. The effect of resistin to attenuate bradykinin-induced vasodilation persisted in the presence of L-NAME or indomethacin, suggesting resistin may act at cell signaling point upstream of NO or PGI2 production. Resistin-induced endothelial dysfunction is not generalized, nor is it consistent with effects mediated by O2- or interference with NO/ PGI2 signaling. The site of the resistin-induced impairment is unknown, but may be at the bradykinin receptor or closely associated signal transduction machinery proximal to NO synthase or cyclooxygenase.
This article has been cited by other articles:
|
|
 |
|
  Z. Bagi Mechanisms of coronary microvascular adaptation to obesity Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2009; 297(3): R556 - R567. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. A. Payne, H. G. Bohlen, U. D. Dincer, L. Borbouse, and J. D. Tune Periadventitial adipose tissue impairs coronary endothelial function via PKC-{beta}-dependent phosphorylation of nitric oxide synthase Am J Physiol Heart Circ Physiol, July 1, 2009; 297(1): H460 - H465. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M.-J. Lee, H. Lin, C.-W. Liu, M.-H. Wu, W.-J. Liao, H.-H. Chang, H.-C. Ku, Y.-S. Chien, W.-H. Ding, and Y.-H. Kao Octylphenol stimulates resistin gene expression in 3T3-L1 adipocytes via the estrogen receptor and extracellular signal-regulated kinase pathways Am J Physiol Cell Physiol, June 1, 2008; 294(6): C1542 - C1551. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Sorop, D. Merkus, V. J. de Beer, B. Houweling, A. Pistea, E. O. McFalls, F. Boomsma, H. M. van Beusekom, W. J. van der Giessen, E. VanBavel, et al. Functional and Structural Adaptations of Coronary Microvessels Distal to a Chronic Coronary Artery Stenosis Circ. Res., April 11, 2008; 102(7): 795 - 803. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. D. Knudson, G. M. Dick, and J. D. Tune Adipokines and Coronary Vasomotor Dysfunction Experimental Biology and Medicine, June 1, 2007; 232(6): 727 - 736. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
