Coronary arterial smooth muscle is myogenically active, is acted upon by a variety of modulating agents, and is subjected, in situ, to compression and distension by the myocardium. Its mechanical properties thus play a key role in the regulation of coronary blood flow. To describe these, we applied phase-plane analysis of shortening velocity vs. length and load clamping to strips of isolated coronary arteries made to contract by an increase in extracellular potassium concentration. At any load, length was larger in relaxed than in "resting" preparations. In addition, preloaded shortening was smaller than would be expected from the relation between active isometric force and muscle length. These suggest the occurrence of stretch-activation and shortening-inactivation. To judge from both phase-plane analysis and quick release experiments, shortening velocity depended on load as well as on time. Velocity decreased with increasing duration of contraction. Shortened coronary arteries resisted lengthening induced by loading and could transiently bear loads that considerably exceeded isometric force. This load-bearing capacity increased with increasing shortening. In conclusion, coronary arterial smooth muscle displays the classical relationship between length, force, and velocity. However, the nature of this relationship changes with duration of activity. In addition, it is greatly affected during changes in length or load, such as expected when the arterial wall is exposed to pulsatile blood flow and is surrounded by mechanically active muscle.