chapter  8
56 Pages

Pathogenesis of Catecholamine-Induced Cardiomyopathy

ByNaranjan S. Dhalla, Melissa R. Dent, Amarjit S. Arneja

Naranjan S. Dhalla, Melissa R. Dent, and Amarjit S. Arneja

Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, and Departments of Physiology and Internal Medicine, Faculty of

Medicine, University of Manitoba, Winnipeg, Canada

INTRODUCTION

Activation of the sympathetic nervous system (SNS) in response to stress

releases catecholamines from the sympathetic nerve endings and adrenal

medulla. Catecholamines, such as epinephrine, norepinephrine, and dopamine,

are the major components that are released endogenously because of stressful

stimuli, whereas isoproterenol is a synthetic catecholamine that simulates

the actions of SNS activation on the heart. The adrenergic receptors in the heart

that are stimulated by catecholamines are the a-adrenoceptors and b-adrenoceptors (b1 and b2); however, the b2-adrenoceptors are found chiefly in extracardiac sites, such as arterioles, where they cause dilation. On the other hand, the

a-adrenoceptors present in the vascular smooth muscle are mainly concerned with the maintenance of blood vessel tone. SNS activation results in increased

cardiac contraction, increased heart rate, increased systolic blood pressure,

and decreased diastolic pressure. Catecholamines at low concentration are

beneficial in regulating heart function by exerting a positive inotropic action on

the myocardium (1), whereas high concentrations of catecholamines or chronic

exposure to catecholamines over a prolonged period produce deleterious effects

on the cardiovascular system.