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Am J Physiol Heart Circ Physiol 285: H1340-H1346, 2003. First published May 8, 2003; doi:10.1152/ajpheart.01119.2002
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Neuronal control of heart rate in isolated mouse atria

J. K. Choate and R. Feldman

Department of Physiology, Monash University, Victoria 3800, Australia

Submitted 2 January 2003 ; accepted in final form 21 April 2003

A novel mouse isolated atrial preparation with intact postganglionic autonomic innervation was used to investigate the neuronal control of heart rate. To establish whether autonomic activation was likely to alter heart rate by modulating the hyperpolarization-activated current (If), the L-type Ca2+ current (ICa,L), or the ACh-activated K+ current (IK,ACh), the effects of nerve stimulation (right stellate ganglion or right vagus, 1–30 Hz) and autonomic agonists (0.1 µM norepinephrine or 0.3 µM carbachol) on heart rate were investigated in the presence of inhibitors of these currents, cesium chloride (Cs+, 1 mM), nifedipine (200 nM), and barium chloride (Ba2+, 0.1 mM), respectively. The positive chronotropic response to stellate ganglion stimulation was reduced by ~20% with Cs+ and nifedipine (P < 0.05), whereas the heart rate response to norepinephrine was only reduced with Cs+ (P < 0.05). Ba2+ attenuated the decrease in heart rate with vagal stimulation and carbachol by ~60% (P < 0.05). These results are consistent with the idea that sympathetic nerve stimulation modulates If to increase heart rate in the mouse. Activation of ICa,L also appears to contribute to the sympathetic heart rate response. However, the decrease in heart rate with vagal stimulation or carbachol is likely to result primarily from the activation of IK,ACh.

sinoatrial node; heart rate; sympathetic; parasympathetic


Address for reprint requests and other correspondence: J. K. Choate, Dept. of Physiology, PO Box 13F, Monash Univ., Victoria 3800, Australia (E-mail: julia.choate{at}med.monash.edu.au).






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