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Changes in cardiac sympathetic activity in rats after myocardial infarction
Author(s) -
Drobysheva Anastasia,
Ahmad Monir,
Wang Hongwei,
Leenen Frans
Publication year - 2011
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.25.1_supplement.828.6
Cardiac sympathetic hyperactivity plays a major role in the progression of heart failure after myocardial infarction (MI). Little is known about molecular mechanisms that underlie changes in cardiac sympathetic drive post MI. Objective assess changes in Norepinephrine transporter (NET) and Tyrosine hydroxylase (TH) gene and protein expression in stellate ganglia and the heart at 1 and 4 wks after MI in rats. Wistar rats underwent either coronary artery ligation or sham surgery. Mean MI size estimated by echocardiography was 35%. Gene and protein expression was assessed by RT‐qPCR and Western blotting. Protein gene product 9.5 (PGP 9.5) was used as a neuronal marker to account for innervation density. PGK and B‐actin were used as housekeeping genes in RT‐qPCR and Western blotting. mRNA in stellate gangliaTH/PGK NET/PGK 1 wk 4 wks 1 wk 4 wksLeft SG Sham (n=4) 1.2±0.03 1.0±0.04 2.0±0.3 1.9±0.3 MI (n=5) 1.4±0.04 1.2±0.03 2.2±0.3 2.1±0.3 Right SG Sham (n=4) 0.9±0.03 0.7±0.07 1.8±0.2 1.3±0.2 MI (n=5) 1.2±0.03 1.3±0.16 * 2.0±0.3 2.3±0.2 *Protein in the base of the heartTH/B‐actin NET/B‐actin PGP/B‐actinSham (n=6) MI (n=7) Sham (n=6) MI (n=7) Sham (n=6) MI (n=7)1wk 4.5±0.6 3.6±0.3 3.2±0.1 3.3±0.1 0.9±0.1 1.9±0.3 * 4 wks 3.3±0.4 3.5±0.7 2.1±0.1 2.2±0.1 0.6±0.1 1.0±0.1 *Data shown as mean ±SE. * P < 0.05, vs. shamIn Wistar rats post MI there is rapid and persistent sympathetic hyperinnervation in the base of the heart, followed by a selective increase of TH and NET gene expression in the RSG. RSG predominantly innervate the left ventricle and this activation may contribute to sympathetic hyperactivity in the left ventricle post MI. Supported by operating grant FRN: MOP 13182 from the Canadian Institutes of Health Research.