AJP - Heart and Circulatory Physiology, Vol 249, Issue 3 463-H469, Copyright © 1985 by American Physiological Society
Nicotine increases heart adenosine release, oxygen consumption, and contractility
R. A. Fenton and J. G. Dobson Jr
The effect of nicotine on adenosine release, oxygen consumption, and
contractility was investigated in perfused rat hearts. Continuous infusion
of nicotine into the perfusing physiological saline (PS) elicited a
propranolol (10(-6) M) sensitive transient elevation of developed left
ventricular pressure (LVP) and maximum rates of left ventricular pressure
development and relaxation (+/- dP/dtmax) within 20 s, which subsequently
declined to maintained elevated plateau levels by 1 min. The continuous
infusions of nicotine to achieve PS concentrations of 5 X 10(-4), 1 X
10(-4), or 5 X 10(-5) M, respectively resulted in significant increases in
the mean plateau levels of LVP (33.4, 10.1, or 6.3%), +dP/dtmax (26.3,
10.8, or 6.9%) and-dP/dtmax (35.0, 11.9, or 9.0%) at 1 min. The inclusion
of propranolol (10(-6) M) with or without atropine (10(-6) M) did not alter
these maintained plateau responses to nicotine. During the plateau phase of
the contractile response oxygen consumption of the hearts was significantly
elevated by 36, 19, or 11%, and mean levels for adenosine in the coronary
effluent rose by 261, 76, or 74% in response to 5 X 10(-4), 1 X 10(-4), or
5 X 10(-5) M nicotine, respectively. Nicotine did not influence
[14C]adenosine uptake by the hearts. These results suggest that nicotine is
capable of 1) augmenting cardiac contractility and oxygen consumption
independent of beta-adrenergic or muscarinic influence, and 2) elevating
the appearance of adenosine in the coronary circulation presumably by
enhancing myocardial production of the nucleoside.
