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Altered calcium sensitivity contributes to enhanced contractility of collateral-dependent coronary arteries

¹Department of Biomedical Sciences, ²Dalton Cardiovascular Research Center, ³Departments of Medical Pharmacology and Physiology and of Internal Medicine, University of Missouri, Columbia, Missouri 65211; and ⁴Department of Medical Physiology, The Texas A&M University System Health Sciences Center, College Station, Texas 77843

Submitted 28 December 2003 ; accepted in final form 17 February 2004

Coronary arteries distal to chronic occlusion exhibit enhanced vasoconstriction and impaired relaxation compared with nonoccluded arteries. In this 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 wk after Ameroid placement. Contractile responses to depolarization (10–100 mM KCl) were significantly enhanced in LCX compared with size-matched LAD arterial rings [concentration of KCl causing 50% of the maximal contractile response (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 LCX compared with LAD (–5.29 ± 0.42 vs. –5.68 ± 0.55 pA/pF, respectively). Furthermore, whereas 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 LCX compared with LAD in response to KCl 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 depolarization, independent of changes in whole cell peak Ca²⁺ channel current. Unaltered Ca²⁺ sensitivity in endothelin-stimulated arteries suggests more than one mechanism regulating Ca²⁺ sensitization in coronary smooth muscle.

smooth muscle; Ca²⁺ current; Ca²⁺ channel; voltage clamp; fura 2

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