ALTERED CONTROL OF CALCIUM IN CORONARY SMOOTH-MUSCLE CELLS BY EXERCISE TRAINING

The increase in myoplasmic free Ca (Ca-m) is a primary trigger of cont raction in vascular smooth muscle. We review data showing that the sar coplasmic reticulum (SR) can buffer (attenuate) increases in Ca-m by: 1) sequestering a fraction of Ca entering the cell via sarcolemmal inf lux pathways, and 2) slowly releasing Ca from the SR toward the sarcol emma for extrusion from the cell, thereby decreasing subsequent agonis t-induced Ca-m transients and contraction-so called ''SR Ca unloading. '' Endurance exercise trained (EX), not sedentary (SED), Yucatan minia ture pigs show SR Ca unloading via a ryanodine-sensitive SR Ca release pathway. The slow release of Ca from SR of EX cells may allow for eff lux from the cell by close functional association with sarcolemmal Ca efflux mechanisms. In contrast, rapid, bolus release and resequestrati on of Ca by the SR of SED cells prevents Ca efflux from the cell. The endothelin-sensitive SR Ca store, a subset of the caffeine- and ryanod ine-sensitive SR, is decreased in EX cells. Mildly increased resting C a-m in EX cells may reflect a constant leak of Ca from the SR. The end othelin-sensitive SR Ca store was loaded above basal levels by depolar ization-induced Ca influx. Collectively, these data indicate altered C a-m regulation by the SR in coronary artery of EX animals. Future stud ies should focus on the molecular mechanisms of altered Ca-m regulatio n.