Comparison of Skeletal, Smooth, and Cardiac Muscle
- Skeletal muscle and cardiac muscle are striated, whereas smooth muscle is not striated.
- The skeletal-muscle action-potential upstroke is produced by inward sodium ion (Na⁺) current.
- The skeletal-muscle action potential lasts about 1 millisecond.
- The smooth-muscle action-potential upstroke is produced by inward calcium ion (Ca²⁺) current.
- The smooth-muscle action potential lasts about 10 milliseconds.
- The sinoatrial node cardiac action-potential upstroke is produced by inward calcium ion (Ca²⁺) current.
- Atrial, ventricular, and Purkinje fiber cardiac action-potential upstrokes are produced by inward sodium ion (Na⁺) current.
- Sinoatrial node action potentials have no plateau.
- Atrial, ventricular, and Purkinje fiber action potentials have calcium ion (Ca²⁺)-dependent plateaus.
- A plateau is a prolonged phase of an action potential in which the membrane remains depolarized longer than it would during a brief spike.
- Sinoatrial node and atrial action potentials last about 150 milliseconds.
- Ventricular and Purkinje fiber action potentials last about 250 to 300 milliseconds.
- In skeletal muscle, the action potential depolarizes transverse tubules and causes calcium ion (Ca²⁺) release from nearby sarcoplasmic reticulum.
- Skeletal-muscle contraction is regulated by calcium ion (Ca²⁺) binding to troponin C.
- In smooth muscle, action potentials, hormones, and neurotransmitters can increase intracellular calcium ion (Ca²⁺) through membrane channels or inositol 1,4,5-trisphosphate (IP3)-gated sarcoplasmic-reticulum channels.
- Smooth-muscle contraction is regulated by calcium ion (Ca²⁺) binding calmodulin and activating myosin light-chain kinase.
- In cardiac muscle, inward calcium ion (Ca²⁺) current during the action-potential plateau causes calcium-induced calcium ion release from the sarcoplasmic reticulum.
- Cardiac-muscle contraction is regulated by calcium ion (Ca²⁺) binding to troponin C.
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