In smooth muscle, contraction is initiated by Ca²⁺-calmodulin activation of myosin light chain kinase (MLCK). The mechanism by which alpha-smooth muscle cells sustain tonic contraction at low energy cost (latch state) involves:

• A Prolonged elevation of intracellular Ca²⁺ sustains MLCK activity at full rate throughout tonic contraction, but ATP cost is reduced by mitochondrial proximity
• B Dephosphorylated crossbridges remain slowly cycling or attached (latch bridges), generating force with minimal ATP hydrolysis as myosin light chain phosphatase acts ✓
• C Caldesmon replaces phosphorylated myosin in tonic contraction, using caldesmon-actin bridges that do not require ATP hydrolysis
• D cAMP-independent activation of MLCK by calmodulin kinase IV sustains phosphorylated myosin during the latch state

Explanation

The 'latch state' of smooth muscle describes a condition where sustained force is maintained with lower [Ca²⁺] and minimal ATP consumption compared to the initial activation phase. As intracellular Ca²⁺ declines, MLCK activity decreases and myosin light chain phosphatase (MLCP) dephosphorylates myosin regulatory light chains. However, dephosphorylated crossbridges that are already attached detach very slowly — these 'latch bridges' can maintain tension at a fraction of the energy cost. This explains how vascular smooth muscle and visceral smooth muscle can sustain prolonged tone without fatigue or excessive ATP expenditure. Caldesmon modulates actin-myosin interaction but the latch state primarily depends on slowly cycling dephosphorylated crossbridges.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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