Adrenal release of catecholamines in the coronary and myocardial response to nicotine

The role of cardiac neural stimulation in the absence of direct effects of nicotine and other circulating factors was evaluated by perfusing a region of left ventricular myocardium with blood from a reservoir during systemic nicotine infusion. In normally perfused myocardium, contractile function increased, but in reservoir-perfused myocardium, function deteriorated. To evaluate direct effects of nicotine on myocardial contractile function, nicotine was infused directly into a perfused coronary artery. An intracoronary concentration of nicotine equivalent to that caused by intravenous administration (0.69 +/- 0.08 micrograms per ml plasma) had no effect on myocardial contractile function. An intracoronary nicotine concentration of 5 micrograms/ml was required to directly increase contractile function to approximately the same extent observed during intravenous nicotine. To evaluate the role of circulating catecholamines in the myocardial contractile response to intravenous nicotine, observations were made before and after bilateral adrenalectomy. Adrenalectomy markedly attenuated the pressor response to intravenous nicotine and abolished the positive cardiac inotropic response. We conclude that the adrenal release of catecholamines is primarily responsible for increased myocardial contractile function during intravenous nicotine.