In smooth muscle, tonic contraction is maintained after initial Ca2+ signalling through which mechanism that is absent in skeletal muscle?

• A Smooth muscle has ryanodine receptors that sustain Ca2+ release from SR for prolonged periods without refilling
• B Smooth muscle calmodulin has a 100-fold higher Ca2+ affinity than skeletal muscle troponin C, allowing contraction at negligible Ca2+ levels
• C Smooth muscle uses titin-based passive force generation once Ca2+ triggers initial cross-bridge formation
• D Phosphorylation of myosin light chain (MLC) by MLCK keeps myosin in the latch state; even after Ca2+ returns to baseline, phosphorylated cross-bridges can remain attached (latch-bridge mechanism) through MLCP inhibition by thin filament proteins ✓

Explanation

In smooth muscle, the latch-bridge mechanism allows sustained tonic contraction at low energy cost. Elevated Ca2+ activates calmodulin, which binds MLCK, phosphorylating MLC at Ser19; this enables cross-bridge cycling (contraction). The key additional feature of smooth muscle is that once some cross-bridges form and Ca2+ subsequently falls, myosin light-chain phosphatase (MLCP) dephosphorylates MLC, but dephosphorylated cross-bridges can enter a 'latch state' in which they detach very slowly from actin, maintaining force at minimal ATP cost. Receptor-activated inhibition of MLCP (via ROCK, PKC) further sustains phosphorylation. This is the basis of maintained vascular tone and is distinct from skeletal muscle, where troponin I and troponin C solely regulate actomyosin interaction. Options B–D are not the primary mechanism.

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

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