Smooth-Muscle Excitation-Contraction Coupling
- Smooth-muscle contraction differs from skeletal-muscle contraction because smooth muscle lacks troponin.
- Smooth muscle uses calcium ion (Ca²⁺) to regulate myosin on the thick filament rather than using troponin to regulate actin.
- Depolarization opens voltage-gated calcium ion (Ca²⁺) channels in smooth muscle.
- Voltage-gated calcium ion (Ca²⁺) channels allow extracellular calcium ions to enter smooth-muscle cells.
- Hormones and neurotransmitters can open ligand-gated calcium ion (Ca²⁺) channels in smooth muscle.
- Calcium ion (Ca²⁺) entry can trigger additional calcium ion release from the sarcoplasmic reticulum.
- Inositol 1,4,5-trisphosphate (IP3) gated channels can release calcium ion (Ca²⁺) directly from the sarcoplasmic reticulum in response to hormones and neurotransmitters.
- Inositol 1,4,5-trisphosphate (IP3) is an intracellular signaling molecule that can open calcium-release channels in the sarcoplasmic reticulum.
- Calmodulin is a calcium-binding protein that helps activate smooth-muscle contraction.
- Increased intracellular calcium ion (Ca²⁺) binds calmodulin.
- The calcium ion (Ca²⁺) and calmodulin complex activates myosin light-chain kinase.
- Myosin light-chain kinase phosphorylates myosin and permits myosin to bind actin.
- Phosphorylation is the addition of a phosphate group to a molecule.
- Smooth-muscle cross-bridge cycling produces tension in proportion to intracellular calcium ion (Ca²⁺) concentration.
- Smooth-muscle relaxation occurs when intracellular calcium ion (Ca²⁺) decreases.
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