title: Calcium buffering in coronary smooth muscle after chronic occlusion and exercise training.
abstract: OBJECTIVE
  Exercise promotes "sarcoplasmic reticulum (SR) Ca2+ unloading" in porcine coronary smooth muscle, resulting in decreased agonist-induced Ca2+ release. We studied Ca2+ handling in healthy, non-occluded right coronary artery cells from hearts chronically occluded at the circumflex artery.
  
  
  METHODS
  Myoplasmic free Ca2+ (Ca(m)) was assessed with fura-2 in cells from sedentary (n=8) and aerobically exercise-trained (n=6) female Yucatan pigs after 6-month circumflex artery ameroid occlusion (OCC) and in cells from non-occluded, sedentary pigs (SED, n=5). First, Ca influx was induced by 80 mM KCl depolarization (priming step) followed by 5 mM caffeine to elicit maximal Ca2+ release and depletion. The SR was Ca-loaded again by depolarization and then exposed to caffeine after 2- or 11-min recovery to compare SR Ca2+ unloading.
  
  
  RESULTS
  Baseline Ca(m), caffeine-induced peak Ca(m), and depolarization-induced maximum Ca(m) were decreased, and depolarization-induced time-to-half-maximum was increased in OCC vs. SED pigs, suggesting a tonic Ca2+ buffering (lowering) effect of occlusion. Exercise did not alter these effects. SR Ca2+ unloading occurred only in SED, as evidenced by decreased caffeine-induced Ca2+ release after 11 min of recovery, and was inhibited by low extracellular Na+.
  
  
  CONCLUSIONS
  SR Ca2+ unloading can be demonstrated in coronary smooth muscle from sedentary pigs using a novel SR Ca2+ unloading protocol, and Ca2+ unloading partly depends on Na+-Ca2+ exchange activity. Furthermore, SR Ca2+ unloading in cells from non-occluded right coronary arteries of chronically circumflex-occluded pig hearts was not altered by exercise, perhaps due to enhanced tonic Ca2+ extrusion versus cells from normal, sedentary animals.
authors.affiliation: Vascular Biology Laboratory, Dalton Cardiovascular Research Center, and Department of Physiology, University of Missouri, Columbia, MO 65211, USA.
authors.forename: J J
authors.initials: JJ
authors.lastname: Jones
authors.forename: N J
authors.initials: NJ
authors.lastname: Dietz
authors.forename: C L
authors.initials: CL
authors.lastname: Heaps
authors.forename: J L
authors.initials: JL
authors.lastname: Parker
authors.forename: M
authors.initials: M
authors.lastname: Sturek
mesh_terms: D000222:Adaptation, Physiological; D000704:Analysis of Variance; D000818:Animals; D002021:Buffers; D002110:Caffeine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D003327:Coronary Disease / Q000378:metabolism*; D003331:Coronary Vessels / Q000187:drug effects; D005260:Female; D023421:Models, Animal; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D010805:Physical Conditioning, Animal; D011189:Potassium Chloride / Q000494:pharmacology; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D019831:Sodium-Calcium Exchanger / Q000378:metabolism; D013556:Swine, Miniature
chemical_list: D002021:Buffers; D019831:Sodium-Calcium Exchanger; D002110:Caffeine; D011189:Potassium Chloride; D002118:Calcium