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Am J Physiol Heart Circ Physiol (May 8, 2003). doi:10.1152/ajpheart.01119.2002
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Submitted on January 2, 2003
Accepted on April 21, 2003

The neuronal control of heart rate in the isolated mouse atria

Julia K. Choate1* and Rebecca R. Feldman1

1 Department of Physiology, Monash University, Melbourne, Victoria, Australia

* To whom correspondence should be addressed. E-mail: julia.choate{at}med.monash.edu.au.

A novel mouse isolated atrial preparation with intact postganglionic autonomic innervation was used to investigate the neuronal control of heart rate. To establish if autonomic activation was likely to alter heart rate by modulating the hyperpolarization-activated If current, the L-type calcium current, ICa,L, or the acetylcholine-activated potassium 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 about 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 about 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.




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