Alterations in cytoplasmic calcium sensitivity during porcine coronary artery contractions as detected by aequorin.

Abstract

Intracellular-Ca2+-force relationships were investigated in porcine epicardial coronary arteries by the simultaneous measurement of aequorin luminescence and isometric force. In response to K+ depolarization and histamine, force and aequorin light rose monophasically. In response to carbachol and serotonin, tonic contractions were accompanied by biphasic aequorin signals consisting of an initial spike followed by a low plateau. Contractions produced by prostaglandin F2.alpha. (PGF2.alpha.) or the endoperoxide analogue U-46619 were accompanied by little or no detectable rise in light. Comparison of steady-state force to steady-state light levels indicated that agonists gave greater force for a given intracellular Ca2+ concentration ([Ca2+]i) compared to that seen during K+ contractures. In Ca2+-free bathing media, carbachol produced a transient contraction accompanied by a transient intracellular Ca2+ spike indicating release of Ca2+ from intracellular storage sites. In Ca2+-free batching media PGF2.alpha. produced a tonic contraction with no detectable change in light. These results suggest that changes in the sensitivity of the contractile apparatus to Ca2+ or other activator systems may be as important a mechanism of contraction as are changes in [Ca2+]i.