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1 Medical Pharmacology & Physiology, University of Missouri, Columbia, Missouri, United States
2 Molecular Physiology & Biological Physics and the Cardiovascular Research Center, University of Virginia, Charlottesville, Virginia, United States; Medical Pharmacology & Physiology, University of Missouri, Columbia, Missouri, United States
3 Cellular & Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, United States; Medical Pharmacology & Physiology, University of Missouri, Columbia, Missouri, United States; Internal Medicine and the Center for Diabetes & Cardiovascular Health, University of Missouri, Columbia, Missouri, United States
* To whom correspondence should be addressed. E-mail: msturek{at}iupui.edu.
Aerobic exercise training is known to have profound cardioprotective effects in disease, yet cellular mechanisms remain largely undefined. We tested the hypothesis that increased sarcoplasmic reticulum Ca2+ buffering and increased voltage-gated Ca2+ channel density underlie coronary smooth muscle intracellular Ca2+ (Ca2+i) dysregulation in diabetic dyslipidemia and that exercise training would prevent these increases. Yucatan swine were maintained: 1) control, 2) alloxan-induced hyperglycemic, 3) high fat/cholesterol fed, 4) hyperglycemic plus high fat/cholesterol fed (diabetic dyslipidemic), and 5) diabetic dyslipidemic plus exercise-trained (treadmill running). After 20 wks, the heart was removed and smooth muscle cells isolated from the right coronary artery. We utilized fura-2 imaging of Ca2+i levels to separate the functional role of the sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) from the Na+-Ca2+ exchanger (NCX) and the plasmalemmal Ca2+-ATPase (PMCA), and whole-cell patch clamp to examine voltage-gated Ca2+ channel current density (i.e. Ca2+ influx). Results indicated that diabetic dyslipidemia impaired plasmalemmal Ca2+ efflux, increased basal Ca2+i levels, increased SERCA protein and sarcoplasmic reticulum Ca2+i buffering, and elicited an ~50% decrease in voltage-gated Ca2+-channel current density. Exercise training concurrent with the diabetic dyslipidemic state restored plasmalemmal Ca2+ efflux, SERCA protein, sarcoplasmic reticulum Ca2+i buffering, and voltage-gated Ca2+-channel current density to control levels. Interestingly, basal Ca2+i levels were significantly lower in the exercise-trained group compared to control. Collectively, these results demonstrate a crucial role for exercise in the prevention of diabetic dyslipidemia-induced Ca2+i dysregulation.
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