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The increase in myoplasmic free Ca (Cam) is a primary trigger of contraction in vascular smooth muscle. We review data showing that the sarcoplasmic reticulum (SR) can buffer (attenuate) increases in Cam by: 1) sequestering a fraction of Ca entering the cell via sarcolemmal influx pathways, and 2) slowly releasing Ca from the SR toward the sarcolemma for extrusion from the cell, thereby decreasing subsequent agonist-induced Cam transients and contraction--so called "SR Ca unloading." Endurance exercise trained (EX), not sedentary (SED), Yucatan miniature 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 efflux from the cell by close functional association with sarcolemmal Ca efflux mechanisms. In contrast, rapid, bolus release and resequestration 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 ryanodine-sensitive SR, is decreased in EX cells. Mildly increased resting Cam in EX cells may reflect a constant leak of Ca from the SR. The endothelin-sensitive SR Ca store was loaded above basal levels by depolarization-induced Ca influx. Collectively, these data indicate altered Cam regulation by the SR in coronary artery of EX animals. Future studies should focus on the molecular mechanisms of altered Cam regulation.
Underwood et al. (1994) studied this question.