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Exercise prevents diabetes-induced impairment in superficial buffer barrier in porcine coronary smooth muscle

Departments of ¹Medical Pharmacology and Physiology ²Internal Medicine, and ³Center for Diabetes and Cardiovascular Health, University of Missouri, Columbia, Missouri 65212

Submitted 2 May 2003 ; accepted in final form 14 November 2003

In healthy coronary smooth muscle cells, the superficial sarcoplasmic reticulum (SR) buffers rise 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. We tested the hypothesis that diabetic dyslipidemia impairs Ca²⁺ extrusion via a decrease in superficial SR and that exercise will prevent these losses. Male Yucatan swine were maintained in four treatment groups: 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 5,6-carboxyeosin, respectively. Superficial SR was quantified using the internal membrane dye 3,3'-dihexyloxacarbocyanine iodide (DiOC₆) and novel analysis techniques. We found that, 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. On the basis of these results, we conclude exercise attenuates the diabetic dyslipidemia-induced impairment in intracellular Ca²⁺ regulation.

sodium-calcium exchanger; plasma membrane calcium-adenosinetriphosphatase; sarco(endo)plasmic reticulum calcium-transporting adenosinetriphosphatase

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