| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR, USA
2 Department of Anesthesiology, Oregon Health & Science University, Portland, OR, USA; Department of Anesthesiology Service, Portland VA Medical Center, Portland, OR, USA
* To whom correspondence should be addressed. E-mail: habecker{at}ohsu.edu.
Regional changes occur in the sympathetic innervation of the heart following myocardial infarction (MI), including loss of norepinephrine (NE) uptake and depletion of neuronal NE. This apparent denervation is accompanied by increased cardiac NE spillover. One potential explanation for these apparently contradictory findings is that the sympathetic neurons innervating the heart are exposed to environmental stimuli that alter neuronal function. To understand the changes that occur in the innervation of the heart following MI, immunohistochemical, biochemical, and molecular analyses were carried out in the heart and stellate ganglia of control and MI rats. Immunohistochemistry with pan-neuronal markers revealed extensive denervation in the left ventricle below the infarct, but sympathetic nerve fibers were retained in the base of the heart. Western blot analysis revealed that tyrosine hydroxylase (TH) expression (normalized to a pan-neuronal marker) was increased significantly in the base of the heart and in the stellate ganglia, but decreased in the left ventricle below the MI. Norepinephrine transporter (NET) binding sites, normalized to total protein, were unchanged except in the left ventricle, where 3H-Nisoxetine binding was decreased. TH mRNA was increased significantly in the left and right stellate ganglia following MI, while NET mRNA was not. In the base of the heart, increased TH coupled with no change in the NE transporter may explain the increase in extracellular NE observed following MI. Coupled with substantial denervation in the left ventricle, these changes likely contribute to the onset of cardiac arrhythmias.
This article has been cited by other articles:
|
|
 |
|
  D. C. Parrish, E. N. Alston, H. Rohrer, S. M. Hermes, S. A. Aicher, P. Nkadi, W. R. Woodward, J. Stubbusch, R. T. Gardner, and B. A. Habecker Absence of gp130 in dopamine {beta}-hydroxylase-expressing neurons leads to autonomic imbalance and increased reperfusion arrhythmias Am J Physiol Heart Circ Physiol, September 1, 2009; 297(3): H960 - H967. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. A. Wehrwein, L. M. Parker, A. A. Wright, J. M. Spitsbergen, M. Novotny, D. Babankova, G. M. Swain, B. A. Habecker, and D. L. Kreulen Cardiac norepinephrine transporter protein expression is inversely correlated to chamber norepinephrine content Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2008; 295(3): R857 - R863. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. C. Parrish, K. Gritman, D. M. Van Winkle, W. R. Woodward, M. Bader, and B. A. Habecker Postinfarct sympathetic hyperactivity differentially stimulates expression of tyrosine hydroxylase and norepinephrine transporter Am J Physiol Heart Circ Physiol, January 1, 2008; 294(1): H99 - H106. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. W. Hewett, L. W. Norman, D. Sedmera, R. J. Barker, C. Justus, J. Zhang, S. W. Kubalak, and R. G. Gourdie Knockout of the neural and heart expressed gene HF-1b results in apical deficits of ventricular structure and activation Cardiovasc Res, August 15, 2005; 67(3): 548 - 560. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
