ABSTRACT
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.
