HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 286/6/H2229    most recent 00768.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (19) Citing Articles via Google Scholar Google Scholar Articles by Li, W. Articles by Habecker, B. A. Search for Related Content PubMed PubMed Citation Articles by Li, W. Articles by Habecker, B. A.

Infarction alters both the distribution and noradrenergic properties of cardiac sympathetic neurons

¹Physiology and Pharmacology and ²Anesthesiology, Oregon Health and Science University, and ³Anesthesiology Service, Portland Veterans Affairs Medical Center, Portland, Oregon 97239

Submitted 14 August 2003 ; accepted in final form 14 January 2004

Regional changes occur in the sympathetic innervation of the heart after 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 after MI, immunohistochemical, biochemical, and molecular analyses were carried out in the heart and stellate ganglia of control and MI rats. Immunohistochemistry with panneuronal markers revealed extensive denervation in the left ventricle (LV) 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 panneuronal marker) was increased significantly in the base of the heart and in the stellate ganglia but decreased in the LV below the MI. NE transporter (NET) binding sites, normalized to total protein, were unchanged, except in the LV, where [³H]nisoxetine binding was decreased. TH mRNA was increased significantly in the left and right stellate ganglia after MI, while NET mRNA was not. In the base of the heart, increased TH coupled with no change in NET may explain the increase in extracellular NE observed after MI. Coupled with substantial denervation in the LV, these changes likely contribute to the onset of cardiac arrhythmias.

tyrosine hydroxylase; norepinephrine transporter; myocardial infarction

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]