Adrenal Release of Catecholamines in the Coronary and Myocardial Response to Nicotine

  • H. Fred Downey
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 273)


Nicotine increases myocardial contractility in the in situ heart (12,15,17,22). Several mechanisms might account for this positive inotropic effect: 1) Stimulation of the myocardium by sympathetic nerves (1,3); 2) Release of catecholamines from cardiac tissue (6,23); 3) Stimulation of the myocardium by nicotine independent of catecholamines (4,12,19); 4) Release of catecholamines from the adrenal glands (2,26,27,28). Each of these mechanisms can be activated under appropriate experimental conditions, but their relative potency and contribution to the integrated cardiac response to intravenous nicotine was uncertain. Thus, we investigated the extent to which the increase in myocardial contractile function could be accounted for independently by cardiac nerve activation or by direct action of intracoronary nicotine. When we found these mechanisms incapable of accounting for the observed cardiac responses to intravenous nicotine, we examined the role of the adrenal glands (11).


Left Anterior Descend Contractile Function Myocardial Oxygen Consumption Beta Adrenergic Blockade Nicotine Infusion 


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Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • H. Fred Downey
    • 1
  1. 1.Department of PhysiologyTexas College of Osteopathic MedicineFort WorthUSA

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