AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 292: H808-H813, 2007. First published September 29, 2006; doi:10.1152/ajpheart.00295.2006
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Interstitial K+ concentration in active muscle after myocardial infarction

Jianhua Li, Zhaohui Gao, Valerie Kehoe, and Lawrence I. Sinoway

Division of Cardiology, Department of Medicine, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania

Submitted 22 March 2006 ; accepted in final form 22 September 2006

Previous work demonstrated that Na+-K+ pump activity within skeletal muscle is attenuated in myocardial infarction (MI). This may lead to enhanced interstitial K+ concentration ([K+]o) in the muscle. We tested the hypothesis that [K+]o rises with muscle contraction and that, in rats with MI, the rate of rise in [K+]o is greater than it is in control animals. Microdialysis probes were inserted in the skeletal muscle of six healthy control and six MI rats. The ends of the probes were then attached to the K+ electrodes, and [K+]o was continuously measured. Muscle contraction was induced by electrical stimulation of the sciatic nerves for 1 min. Stimulation at 1 and 3 Hz increased muscle [K+]o by 14.2% and 44.7% in controls and by 22.9% and 62.8% in MI rats (P < 0.05 vs. controls), respectively. When ouabain, an inhibitor of Na+-K+ pump, was added to the perfusate, muscle [K+]o rose significantly. This effect of ouabain was significantly attenuated in MI animals. In conclusion, when compared with that in control animals, an increase of [K+]o in exercising muscle is augmented in MI rats, likely due to an attenuation of Na+-K+ pump activity.

sympathetic nervous system; exercise; blood flow



Address for reprint requests and other correspondence: J. Li, Penn State Heart and Vascular Inst., Div. of Cardiology, H047, Pennsylvania State Univ. College of Medicine, 500 University Dr., Hershey, PA 17033 (e-mail: jzl10{at}psu.edu)







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