Augmented Ca2+‐activated Ca2+ influx and voltage‐gated Ca2+ entry in coronary vs. peripheral conduit arteries in domestic swine. (LB668)

Intracellular Ca2+ handling has been characterized in a variety of animal models in different vascular beds. However, the extent of regional differences in Ca2+ entry in coronary and peripheral conduit vascular smooth muscle cells (VSM) within an animal model is unknown. VSM were enzymatically isolated from domestic swine coronary (right coronary artery and left anterior descending artery) and peripheral (femoral and popliteal artery) arteries and were digitally imaged using the fluorescent Ca2+ indicator, fura‐2. Cells were exposed to 80 mM K+ in physiologic Ca2+ to assess Ca2+ entry through voltage‐gated Ca2+ channels. Following 80 mM K+ the cells were treated with either physiologic salt solution (PSS) or Ca2+‐free PSS before 5 mM caffeine was used to release intracellular Ca2+ from the sarcoplasmic reticulum (SR). Coronary VSM exhibited a greater response to 80 mM K+ vs. peripheral VSM (2.62±0.03 vs. 2.44±0.04 F360/F380) x minutes). In PSS there was no difference in peak Ca2+ transient elicited by caffeine‐induced Ca2+ store release between coronary and peripheral VSM. In Ca2+‐free PSS peripheral arteries had a smaller caffeine‐induced Ca2+ transient vs. coronary arteries (0.36±0.02 vs. 0.20±0.03 F360/F380). These data suggest SR Ca2+ release elicited greater Ca2+‐activated Ca2+ influx in peripheral artery VSM. Heterogeneous regulation of Ca2+ entry in VSM coronary and peripheral arteries warrants further investigation.Grant Funding Source: NIH R01 HL062552, T32 HL079995