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Regulation of Galanin Expression by Post‐infarct Cardiac Sympathetic Hyperactivity
Author(s) -
Ewert Timothy Jarred,
Gritman Kurt,
Habecker Beth A.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1263-d
Subject(s) - galanin , medicine , endocrinology , neuropeptide , myocardial infarction , sympathetic nervous system , cardiology , blood pressure , receptor
The neuropeptide galanin is elevated in the cardiac sympathetic innervation after myocardial infarction (MI). Galanin inhibits vagal transmission and may support the regeneration of sympathetic nerves, thereby contributing to the development of arrhythmia and sudden cardiac death after MI. The reason for increased galanin production in sympathetic neurons after myocardial infarction is not known. Cardiac sympathetic neurons are activated chronically after MI, and activation of sympathetic neurons in culture stimulates galanin expression. Therefore, we tested the hypothesis that increased sympathetic nerve activity stimulates galanin expression in cardiac sympathetic neurons after myocardial infarction. To test this hypothesis we used AOGEN transgenic rats, which lack brain angiotensinogen and do not exhibit post‐infarct sympathetic hyperactivity. Hearts and stellate ganglia, which contain cardiac sympathetic neurons, were collected from wild‐type and AOGEN rats one week after ischemia‐reperfusion or sham surgery. Real‐Time Polymerase Chain Reaction (PCR) was used to measure galanin mRNA expression in the stellate ganglia and an Enzyme‐Linked Immunosorbent Assay was used to measure galanin peptide content in the heart. Galanin mRNA expression increased approximately 3‐fold after infarct in cardiac sympathetic neurons of both genotypes compared to unoperated and sham controls. Left ventricular galanin content, however, increased only in wild type rats and not in AOGEN rats. These data support the hypothesis that post‐infarct cardiac sympathetic hyperactivity stimulates galanin peptide production, but suggest it does not regulate galanin mRNA expression. Supported by HL68231 and an APS undergraduate fellowship to TJE.