1. Intracellular-Ca2+-force relationships were investigated in porcine epicardial coronary arteries by the simultaneous measurement of aequorin luminescence and isometric force. 2. 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. 3. 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. 4. 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. 5. In Ca2+-free bathing media PGF2 alpha produced a tonic contraction with no detectable change in light. 6. 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.