In vascular smooth muscle, Ca²⁺-calmodulin activates myosin light chain kinase (MLCK), which phosphorylates myosin light chain (MLC20) to initiate contraction. Which mechanism maintains 'latch state' (sustained contraction at low energy cost) in smooth muscle?

• A Sustained Ca²⁺ influx via L-type channels continuously activates MLCK, maintaining phosphorylation
• B PKC phosphorylates caldesmon, preventing tropomyosin from blocking the actin-binding site indefinitely
• C Calponin, when phosphorylated by CaMKII, holds myosin heads in the rigor state indefinitely
• D Dephosphorylated cross-bridges remain attached to actin (latch bridges) after MLCP dephosphorylates MLC; these slowly cycling bridges maintain tension at low ATP consumption ✓

Explanation

The 'latch state' in smooth muscle occurs when myosin light chain phosphatase (MLCP) dephosphorylates MLC20 while the myosin head remains attached to actin. These dephosphorylated but still attached 'latch bridges' cycle extremely slowly, maintaining force with minimal ATP consumption. This mechanism underlies sustained vascular tone and sphincter maintenance. ROCK (Rho-kinase) inhibits MLCP, increasing MLC phosphorylation and contraction; ROCK inhibitors (e.g., fasudil) reduce vascular smooth muscle tone. The latch state explains why smooth muscle can sustain tone for hours without fatigue.

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

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