Angiotensin receptors alter myocardial infarction-induced remodeling of the guinea pig cardiac plexus.

Neurohumoral remodeling is fundamental to the evolution of heart disease. This study examined the effects of chronic treatment with an ACE inhibitor (captopril, 3 mg·kg(-1)·day(-1)), AT1 receptor antagonist (losartan, 3 mg·kg(-1)·day(-1)), or AT2 receptor agonist (CGP42112A, 0.14 mg·kg(-1)·day(-1)) on remodeling of the guinea pig intrinsic cardiac plexus following chronic myocardial infarction (MI).

Dynamic remodeling of the guinea pig intrinsic cardiac plexus induced by chronic myocardial infarction.

Myocardial infarction (MI) is associated with remodeling of the heart and neurohumoral control systems. The objective of this study was to define time-dependent changes in intrinsic cardiac (IC) neuronal excitability, synaptic efficacy, and neurochemical modulation following MI. MI was produced in guinea pigs by ligation of the coronary artery and associated vein on the dorsal surface of the heart.

Remodeling of intrinsic cardiac neurons: effects of β-adrenergic receptor blockade in guinea pig models of chronic heart disease.

Chronic heart disease induces remodeling of cardiac tissue and associated neuronal components. Treatment of chronic heart disease often involves pharmacological blockade of adrenergic receptors. This study examined the specific changes in neuronal sensitivity of guinea pig intrinsic cardiac neurons to autonomic modulators in animals with chronic cardiac disease, in the presence or absence of adrenergic blockage.