Coronary arteries distal to chronic occlusion exhibit enhanced vasoconstriction and impaired relaxation when compared with nonoccluded arteries. In the present study, we tested the hypotheses that an increase in peak Ca²⁺ channel current density and/or increased Ca²⁺ sensitivity contributes to altered contractility in collateral-dependent coronary arteries. Ameroid occluders were surgically placed around the proximal left circumflex coronary artery (LCX) of female miniature swine. Segments of epicardial arteries (~1 mm luminal diameter) were isolated from the LCX and nonoccluded left anterior descending (LAD) arteries 24 wks following Ameroid placement. Contractile responses to depolarization (10-100 mM KCl) were significantly enhanced in LCX compared with size-matched LAD arterial rings (EC₅₀; LAD=41.7±2.3, LCX=34.3±2.7 mM). However, peak Ca²⁺ channel current was not altered in isolated smooth muscle cells from the LCX compared with LAD (-5.29±0.42 vs. -5.68±0.55 pA/pF, respectively). Furthermore, while half-maximal activation of Ca²⁺ channel current occurred at nearly the same membrane potential in LAD and LCX, half-maximal inactivation was shifted to a more positive membrane potential in LCX cells. Simultaneous measures of contractile tension and intracellular free Ca²⁺ (fura-2) levels in arterial rings revealed that significantly more tension was produced per unit change in fura-2 ratio in the LCX compared with the LAD in response to KCl-induced membrane depolarization, but not during receptor-agonist stimulation with endothelin-1. Taken together, our data indicate that coronary arteries distal to chronic occlusion display increased Ca²⁺ sensitivity in response to high KCl-induced membrane-depolarization, independent of changes in whole-cell peak Ca²⁺ channel current. Unaltered Ca²⁺ sensitivity in endothelin-stimulated arterial rings suggests more than one mechanism regulates Ca²⁺ sensitization in coronary smooth muscle.