Answer
Excitation-contraction coupling in smooth muscle differs from that in skeletal muscle in several key ways. The primary differences arise from the absence of the troponin-tropomyosin complex in smooth muscle and the central role of calmodulin and myosin light-chain kinase (MLCK) in regulating smooth muscle contraction:
**Differences in Excitation-Contraction Coupling:**
**1. Lack of Troponin-Tropomyosin Complex**:
- In skeletal muscle, the troponin-tropomyosin complex regulates muscle contraction by blocking myosin-binding sites on actin when the muscle is at rest. Calcium ions (Ca2+) released from the sarcoplasmic reticulum bind to troponin, causing a conformational change that allows myosin to bind to actin and initiate contraction.
- In contrast, smooth muscle lacks the troponin-tropomyosin complex. Instead, calcium regulation and contraction in smooth muscle rely on different mechanisms.
**2. Role of Calmodulin and MLCK**:
- In smooth muscle, the key regulator of contraction is calmodulin, a calcium-binding protein that is abundant in smooth muscle cells.
- When calcium levels increase in the cytoplasm of smooth muscle cells, calcium ions bind to calmodulin, forming a calcium-calmodulin complex.
- The calcium-calmodulin complex activates myosin light-chain kinase (MLCK), an enzyme that phosphorylates the myosin light chains of myosin II.
**3. Myosin Light-Chain Phosphorylation**:
- In smooth muscle, contraction is initiated by the phosphorylation (addition of phosphate groups) of myosin light chains by activated MLCK.
- Phosphorylation of myosin light chains allows myosin to bind to actin and initiate the cross-bridge cycling and sliding of actin and myosin filaments, leading to muscle contraction.
- The dephosphorylation of myosin light chains, catalyzed by myosin light-chain phosphatase (MLCP), leads to muscle relaxation.
**4. Slow Onset and Sustained Contractions**:
- Excitation-contraction coupling in smooth muscle often has a slower onset compared to skeletal muscle.
- Smooth muscle contractions can be sustained for longer periods because myosin light-chain phosphorylation is maintained as long as calcium-calmodulin complexes are present.
**5. Regulation by Membrane Potential and Hormones**:
- The membrane potential of smooth muscle cells can be influenced by factors such as hormones, neurotransmitters, and stretch.
- Changes in membrane potential can lead to calcium influx through voltage-gated calcium channels, which can then initiate the excitation-contraction coupling process.
In summary, the primary difference in excitation-contraction coupling between smooth muscle and skeletal muscle lies in the absence of the troponin-tropomyosin complex in smooth muscle and the pivotal role played by calmodulin and MLCK in regulating smooth muscle contraction. When calcium levels rise, calmodulin activates MLCK, which, in turn, phosphorylates myosin light chains to initiate muscle contraction. This unique mechanism allows smooth muscle to contract slowly and maintain tension for extended periods, making it well-suited for functions like controlling blood vessel diameter and peristaltic movements in the digestive tract.
Work Step by Step
Excitation-contraction coupling in smooth muscle differs from that in skeletal muscle in several key ways. The primary differences arise from the absence of the troponin-tropomyosin complex in smooth muscle and the central role of calmodulin and myosin light-chain kinase (MLCK) in regulating smooth muscle contraction:
**Differences in Excitation-Contraction Coupling:**
**1. Lack of Troponin-Tropomyosin Complex**:
- In skeletal muscle, the troponin-tropomyosin complex regulates muscle contraction by blocking myosin-binding sites on actin when the muscle is at rest. Calcium ions (Ca2+) released from the sarcoplasmic reticulum bind to troponin, causing a conformational change that allows myosin to bind to actin and initiate contraction.
- In contrast, smooth muscle lacks the troponin-tropomyosin complex. Instead, calcium regulation and contraction in smooth muscle rely on different mechanisms.
**2. Role of Calmodulin and MLCK**:
- In smooth muscle, the key regulator of contraction is calmodulin, a calcium-binding protein that is abundant in smooth muscle cells.
- When calcium levels increase in the cytoplasm of smooth muscle cells, calcium ions bind to calmodulin, forming a calcium-calmodulin complex.
- The calcium-calmodulin complex activates myosin light-chain kinase (MLCK), an enzyme that phosphorylates the myosin light chains of myosin II.
**3. Myosin Light-Chain Phosphorylation**:
- In smooth muscle, contraction is initiated by the phosphorylation (addition of phosphate groups) of myosin light chains by activated MLCK.
- Phosphorylation of myosin light chains allows myosin to bind to actin and initiate the cross-bridge cycling and sliding of actin and myosin filaments, leading to muscle contraction.
- The dephosphorylation of myosin light chains, catalyzed by myosin light-chain phosphatase (MLCP), leads to muscle relaxation.
**4. Slow Onset and Sustained Contractions**:
- Excitation-contraction coupling in smooth muscle often has a slower onset compared to skeletal muscle.
- Smooth muscle contractions can be sustained for longer periods because myosin light-chain phosphorylation is maintained as long as calcium-calmodulin complexes are present.
**5. Regulation by Membrane Potential and Hormones**:
- The membrane potential of smooth muscle cells can be influenced by factors such as hormones, neurotransmitters, and stretch.
- Changes in membrane potential can lead to calcium influx through voltage-gated calcium channels, which can then initiate the excitation-contraction coupling process.
In summary, the primary difference in excitation-contraction coupling between smooth muscle and skeletal muscle lies in the absence of the troponin-tropomyosin complex in smooth muscle and the pivotal role played by calmodulin and MLCK in regulating smooth muscle contraction. When calcium levels rise, calmodulin activates MLCK, which, in turn, phosphorylates myosin light chains to initiate muscle contraction. This unique mechanism allows smooth muscle to contract slowly and maintain tension for extended periods, making it well-suited for functions like controlling blood vessel diameter and peristaltic movements in the digestive tract.
