The properties of cardiac contractile proteins are modulated by autonomic innervation.

The force generators in myocardial cells of rats and rabbits can exist in three different states: relaxed and calcium unresponsive; relaxed and calcium responsive; and contracted. The transition between the two calcium responsive states is produced by the abrupt rise in the concentration of calcium ions during activation by depolarization of the surface membrane. The transition between the two relaxed states is controlled by the beta-adrenergic system. Stimulation converts calcium unresponsive to calcium responsive force generators by causing the release of a 21,000 dalton regulatory factor from intracellular sites on a membrane. The factor then interacts with myosin. The regulatory system can distinguish between V1 and V3 myosins, producing a calcium responsive state in the former and a calcium unresponsive state in the latter. The result of beta-adrenergic activity is, therefore, an increase in the faster and a decrease in the slower force generators. As a result individual cardiac cells can have many different force-velocity relations.