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

B. R. Wamhoff, D. K. Bowles, N. J. Dietz, Q. Hu, M. Sturek

Research output: Contribution to journalArticle

30 Scopus citations


Physical inactivity is an independent risk factor for coronary heart disease, yet the mechanism(s) of exercise-related cardioprotection remains 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 with sedentary (SED) swine (P < 0.01). EX decreased single cell peak endothelin-1-induced cytosolic Ca2+ responses compared with SED by 16% and peak nuclear Ca2+ responses by 33% (P < 0.05), as determined by confocal microscopy. On the basis of these results, we hypothesized that sarco(endo)plasmic reticulum 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.

Original languageEnglish (US)
Pages (from-to)H2397-H2410
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number6 52-6
StatePublished - Dec 1 2002


  • Electron microscopy
  • Endothelin-1
  • Fluorescence microscopy
  • Sarco(endo)plasmic reticulum Ca-ATPase
  • Swine

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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