Smooth muscle contraction !
- Mechanism
- Exam priority: medium
Smooth muscle in vessels, airways and gut squeezes slowly and can hold tone for hours using very little energy.
Updated 2026-11-01
Also called: Calmodulin–MLCK pathway, Latch state
See it in 3D: Trachea · Stomach · Urinary bladder
What it is
Smooth muscle lines blood vessels, airways, the gut, bladder and uterus. Its contraction is switched on when Ca²⁺ binds calmodulin and activates myosin light-chain kinase (MLCK), which phosphorylates myosin. Myosin phosphatase reverses this, so tone reflects the balance between the two, set by nerves, hormones, stretch and local factors such as nitric oxide.
How it works, step by step
- A stimulus (α1 or M3 receptor agonist, stretch, depolarization) raises cytosolic Ca²⁺.
- Gq-coupled receptors activate phospholipase C, producing IP₃ (SR Ca²⁺ release) and DAG.
- Depolarization opens L-type Ca²⁺ channels, adding extracellular Ca²⁺.
- Four Ca²⁺ ions bind calmodulin; the complex activates myosin light-chain kinase.
- MLCK phosphorylates the regulatory light chain, enabling myosin to cycle on actin anchored to dense bodies.
- Myosin phosphatase removes the phosphate; slowly detaching heads give the latch state and sustained tone.
- Ca²⁺ is removed by SERCA, plasma membrane Ca²⁺-ATPase and Na⁺/Ca²⁺ exchange, and the muscle relaxes.
Regulation
- +Norepinephrine on α1 receptors (Gq): IP₃ and Ca²⁺ rise: vasoconstriction
- +Acetylcholine on M3 receptors (Gq): Bronchoconstriction, gut and bladder contraction
- +Stretch (myogenic response): Arterioles constrict when pressure rises (autoregulation)
- −β2 agonists (Gs → cAMP): Lower Ca²⁺ and MLCK activity: bronchodilation
- −Nitric oxide (cGMP): Activates myosin phosphatase: vasodilation
Clinical notes
- Asthma: airway smooth muscle is hyperresponsive; inhaled β2 agonists relax it via cAMP, and anticholinergics block M3-driven constriction.
- Arterial hypertension: increased vascular tone and remodeling raise peripheral resistance; Ca²⁺ channel blockers and α1 blockers lower tone.
- Nitrates and phosphodiesterase-5 inhibitors act through the NO–cGMP pathway; combining them can drop blood pressure dangerously.
Test yourself
Think of the answer, then tap the question to see it.
How does a β2 agonist relax bronchial smooth muscle at the molecular level?
β2 receptors activate Gs and adenylyl cyclase; cAMP activates PKA, which lowers cytosolic Ca²⁺ and phosphorylates MLCK so it is less active. Less myosin phosphorylation means relaxation.
Why can smooth muscle hold tone for hours while using far less ATP than skeletal muscle?
In the latch state dephosphorylated cross-bridges remain attached and detach very slowly, so force is kept with little cycling and little ATP use.
Why are nitrates and phosphodiesterase-5 inhibitors dangerous together?
Nitrates raise cGMP via NO and PDE-5 inhibitors stop cGMP breakdown. The combined vasodilation can cause severe hypotension.
How can vascular tone rise without any increase in cytosolic Ca²⁺?
Through Ca²⁺ sensitization: RhoA/Rho kinase inhibits myosin phosphatase, so myosin stays phosphorylated at the same Ca²⁺ level.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Skeletal, cardiac and smooth muscle compared
- Adrenergic and cholinergic receptors
- Sliding filaments and the cross-bridge cycle
- Sympathetic and parasympathetic effects on each organ
Related conditions
In Biochemistry
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 10.8 Smooth Muscle (OpenStax (Rice University), 2022); Asthma (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 8). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
Spotted a mistake?We are always improving for the community. Tell us what is wrong and our team will review it.Report a mistake
Representative model, for educational purposes only.