APPS November 2002 Meeting Abstract 2440


K.A. Whyte, D.J. Adams, School of Biomedical Sciences, University of Queensland, Brisbane, QLD 4072.

Reactive oxygen species (ROS) are produced as by-products of oxidative metabolism. ROS occur in the heart during ischaemia and coronary artery reperfusion, and have been implicated in cardiac dysfunction1,2. The proximity of the intracardiac ganglia (ICG) to the coronary blood supply makes them susceptible to the effects of ROS and it has been shown that hypoxia and post-ischaemic reperfusion influence the neuronal firing activity of ICG3. The present study investigated the effects of ROS upon voltage-sensitive calcium channels (VSCCs) and the delayed rectifier potassium channel in isolated neurones of rat neonatal and adult ICG using the dialyzed whole-cell recording configuration of the patch clamp technique. Bath application of ROS donor, hydrogen peroxide (H2O2, 1 mM), inhibited the VSCC current and shifted the current-voltage (I-V) relationship to more hyperpolarized potentials in both neonatal and adult ICG. In contrast, H2O2 increased the amplitude of the delayed rectifier potassium current in neonatal ICG. Bath application of superoxide dismutase (SOD, 100 U/ml), a scavenger of ROS, to neonatal ICG also inhibited the VSCC current and shifted the I-V relationship to more depolarized potentials. Furthermore, in neonatal ICG, application of SOD prior to H2O2 attentuated the hyperpolarizing shift but not the inhibition of VSCC by H2O2. In contrast, in adult ICG, application of SOD alone had no effect upon either VSCC current amplitude or I-V relationship, but application of SOD prior to H2O2 abolished the hyperpolarizing shift and inhibition by H2O2. These data indicate that the effects of ROS alter depolarization-activated calcium and potassium conductances underlying neuronal excitability of ICG and therefore most likely modify autonomic control of the heart during ischaemia/reperfusion.

(1) Armour JA. Cardiovascular Research. 1999;41:41-54.

(2) Kourie JI. American Journal of Physiology. 1998;275:C1-C24.

(3) Thompson GW, Horackova M, Armour JA. American Journal of Physiology. 1998;275:H1434-1440.

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