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J Appl Physiol (November 21, 2003). doi:10.1152/japplphysiol.00460.2003
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Submitted on May 2, 2003
Accepted on November 14, 2003

Exercise Prevents Diabetes-Induced Impairment in Superficial Buffer Barrier in Porcine Coronary Smooth Muscle

Carol A Witczak1 and Michael Sturek2*

1 Department of Medical Pharmacology & Physiology, University of Missouri, Columbia, MO, USA
2 Department of Medical Pharmacology & Physiology, University of Missouri, Columbia, MO, USA; Department of Internal Medicine, University of Missouri, Columbia, MO, USA; Center for Diabetes & Cardiovascular Health, University of Missouri, Columbia, MO, USA

* To whom correspondence should be addressed. E-mail: SturekM{at}Missouri.edu.

In healthy coronary smooth muscle cells, the superficial sarcoplasmic reticulum (SR) buffers rises in intracellular Ca2+ levels. In diabetic dyslipidemia, basal Ca2+ levels are increased, yet Ca2+ influx is decreased and SR Ca2+-uptake is increased. Exercise prevents diabetic dyslipidemia-induced increases in basal Ca2+ levels and decreases in Ca2+ influx. HYPOTHESIS: Diabetic dyslipidemia impairs Ca2+ extrusion via a decrease in superficial SR, and exercise will prevent these losses. METHODS: Male, Yucatan swine were maintained: control, hyperlipidemic, diabetic dyslipidemic, and diabetic dyslipidemic plus aerobically exercise trained. Intracellular Ca2+ levels were measured during depolarization-induced Ca2+ influx and caffeine-induced SR Ca2+ release. Na+-Ca2+ exchanger and plasmalemmal Ca2+-ATPase activity were assessed by inhibition with low extracellular Na+ and carboxyeosin, respectively. Superficial SR was quantified using the internal membrane dye, 3,3'-dihexyloxacarbocyanine iodide (DiOC6), and novel analysis techniques. RESULTS: In diabetic dyslipidemia, Ca2+ extrusion was impaired and superficial SR was decreased. Exercise prevented the diabetic dyslipidemia-induced decrease in superficial SR and restored plasmalemmal Ca2+ extrusion. CONCLUSION: Exercise attenuates the diabetic dyslipidemia-induced impairment in intracellular Ca2+ regulation.




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