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Inhibition of AT1 receptors alters remodeling of the guinea pig cardiac plexus following chronic MI
Author(s) -
Hardwick Jean C,
Ryan Shan E,
Wilson Matthew J,
Southerland E. Marie,
Ardell Jeffrey L
Publication year - 2012
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.26.1_supplement.1091.3
Subject(s) - losartan , captopril , angiotensin ii receptor type 1 , medicine , endocrinology , angiotensin ii , receptor , blood pressure
Chronic heart disease induces remodeling in the guinea pig intrinsic cardiac plexus, which includes changes in responses to Angiotensin II (Ang II). We examined the role of Ang II in the remodeling process by using chronic treatment with either an AT1 antagonist (Losartan, 3mg/kg/day) or an ACE inhibitor (captopril, 3mg/kg/day) for 6 weeks following surgically‐induced myocardial infarction (MI). Intracellular voltage recordings from individual intracardiac neurons in whole mounts of the cardiac plexus were used to assess changes in physiological responses. Losartan and captopril treatments inhibited the synergistic effects of Ang II on the increase in neuronal excitability with either adrenergic or muscarinic agonists in MI, but did not alter the increase in excitability produced by adrenergic agonists alone. Losartan treatment increased synaptic efficacy for intracardiac neurons in MI animals; captopril did not. These results suggest that Ang II modulates neuronal remodeling post‐MI and that stimulation of AT1 receptors may be involved in the modulation of functional responses in the intrinsic cardiac plexus in the diseased heart.