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Am J Physiol Heart Circ Physiol (July 26, 2002). doi:10.1152/ajpheart.00371.2001
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Articles in PresS, published online ahead of print July 26, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00371.2001
Submitted on May 3, 2001
Accepted on July 16, 2002

Exercise training attenuates coronary smooth muscle phenotypic modulation and nuclear Ca2+ signaling

Brian R Wamhoff, Douglas K Bowles, Nancy J Dietz, Qicheng Hu, and Michael Sturek*

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

Physical inactivity is an independent risk factor for coronary heart disease, yet the mechanism(s) of exercise-related cardioprotection remain unknown. We tested the hypothesis that coronary smooth muscle after exercise training would have decreased mitogen-induced phenotypic modulation and enhanced regulation of nuclear Ca2+. Yucatan swine were endurance exercise trained (EX) on a treadmill for 16-20 wk. EX reduced endothelin-1-induced DNA content by 40% compared to sedentary (SED) swine (p<0.01). EX decreased single cell peak endothelin-1-induced cytosolic Ca2+ responses compared to SED by 16% and peak nuclear Ca2+ responses by 33% (p<0.05), as determined by confocal microscopy. Based on these results, we hypothesized that the SR/ER Ca2+-ATPase (SERCA) and intracellular Ca2+ stores in native smooth muscle are spatially localized to dissociate cytosolic Ca2+ and nuclear Ca2+. Subcellular localization of SERCA in living and fixed cells revealed a distribution of SERCA near the sarcolemma and on the nuclear envelope. These results show that EX enhances nuclear Ca2+ regulation, possibly via SERCA, which may be one mechanism by which coronary smooth muscle cells from EX are less responsive to mitogen-induced phenotypic modulation.




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