Smooth Muscle Physiology PDF

Smooth Muscle Physiology Smooth muscle Smooth muscle is a type of muscle tissue with involuntary contraction capability, typically found in the walls of internal organs. Unlike striated muscles, smooth muscles lack the characteristic striations (sarcomere arrangement) visible under a mi...

Smooth Muscle Physiology Smooth muscle Smooth muscle is a type of muscle tissue with involuntary contraction capability, typically found in the walls of internal organs. Unlike striated muscles, smooth muscles lack the characteristic striations (sarcomere arrangement) visible under a microscope, which is why they are referred to as "smooth." Their contractions are slow, sustained, and involuntary, controlled by the autonomic nervous system and hormonal mechanisms. Characteristics of Smooth Muscle 1. Structural Features 2. Physiological Features 3. Functional Features Characteristics of Smooth Muscle 1. Structural Features: Cell Shape and Structure: Spindle-shaped (fusiform): Wide in the middle, tapered at the ends. Uninucleate: Each cell contains a single nucleus located in the center. Small cell diameter (2-10 µm) and shorter length compared to skeletal muscle cells (20-200 µm). Microscopic Anatomy: Lacks striations due to the absence of sarcomere organization. Actin and myosin filaments are arranged irregularly. Dense bodies: Structures where actin filaments anchor, functioning similarly to Z-discs in striated muscle. 2. Physiological Features: Contraction Mechanism: Calcium-dependent: Calcium influx into the cell is essential for contraction. Contraction is triggered by the myosin light chain kinase (MLCK) enzyme. Contraction is slow but long-lasting and energy-efficient. Involuntary Control: Controlled by the autonomic nervous system (sympathetic and parasympathetic pathways). Hormones and local factors (e.g., oxygen levels, pH, CO₂) can influence contraction. Plasticity: Adapts to prolonged stretching (e.g., during bladder filling). 3. Functional Features: Tonic and Phasic Contractions: Tonic contractions: Maintain constant tension (e.g., regulating blood vessel pressure). Phasic contractions: Periodically contract and relax (e.g., intestinal peristalsis). Slow and Energy-Efficient: ATP consumption is low due to slow myosin ATPase activity. The latch mechanism maintains prolonged contractions with minimal energy usage.  Types of Smooth Muscle 1.Single-Unit (Visceral) Smooth Muscle: 1. Gap junctions between cells enable synchronized contraction. 2. Example: Intestines, uterus. 2.Multi-Unit Smooth Muscle: 1. Cells contract independently as they lack gap junctions. 2. Allows finer control. 3. Example: Iris muscles, arrector pili muscles.  Locations of Smooth Muscle 1.Blood vessel walls: Regulates blood pressure. 2.Digestive system: Enables peristaltic movements. 3.Respiratory tract: Controls bronchial diameter. 4.Urogenital system: Controls contractions in the bladder, ureters, and uterus. 5.Eye: Found in the iris and ciliary muscles. Smooth muscle action potential -50 mV Smooth muscle action potential types 2 type: - Slow wave potential (basal electrical rhythm (BER)) - Spike potentials Spike potentials  Smooth Muscle Action Potential In smooth muscle cells, an action potential is a change in the membrane potential triggered by electrical stimulation. Smooth muscle action potentials differ from those in skeletal muscle and nerve cells, being slower and more prolonged. This process initiates the contraction of smooth muscle.  SLOW WAVE POTENTIALS_ Spontaneous rhythmic fluctuations in the smooth muscle membrane potential Occurs everywhere except the esophagus and proximal stomach Initiated by interstitial cells of Cajal (Pacemaker, ICC) Forms the basis of smooth muscle contraction Coordinates peristalsis Slow waves are not true action potentials but can cause undulating changes in the resting membrane potential BER rarely causes muscle contraction Spike potentials on BER waves increases muscle tension BER rate: 4/min (stomach), 12/min (duodenum), 8/min (distal ileum), 2/min (cecum), 6/min (sigmoid) -50 mV Formation and Phases of the Action Potential 1. Resting Membrane Potential 2. Depolarization (Excitation) 3. Plateau Phase (Optional) 4. Repolarization 5. Sustained Contraction (Latch State) 1. Resting Membrane Potential The resting membrane potential of smooth muscle cells ranges between -50 mV and -60 mV. This value is more positive compared to skeletal muscle and nerve cells. At rest, the membrane is partially permeable to potassium ions, and voltage-gated calcium channels remain closed. Key Players 1.Calcium: Triggers the contraction cascade by activating calmodulin. 2.Calmodulin (CaM): Binds calcium and activates MLCK. 3.Myosin Light Chain Kinase (MLCK): Phosphorylates myosin light chains, enabling contraction. 4.Myosin Light Chain Phosphatase (MLCP): Dephosphorylates myosin, leading to relaxation. Characteristics of Smooth Muscle Action Potential 1. Role of Calcium Calcium is the primary ion involved in smooth muscle action potential. It changes the membrane potential and activates enzymes (e.g., MLCK) that trigger actin-myosin interaction. 2. Slow and Prolonged Smooth muscle action potentials are slower to develop and last longer than those in skeletal muscle and nerve cells. This characteristic supports the energy efficiency and long-duration contractions required by smooth muscles. 3. Spontaneous Activity Some smooth muscles can generate spontaneous action potentials without neural stimulation, such as: Pacemaker cells, which regularly initiate contractions (e.g., intestinal peristalsis controlled by the enteric nervous system). Factors Triggering Smooth Muscle Action Potential 1.Neural Stimulation: 1. The autonomic nervous system (sympathetic and parasympathetic pathways) can initiate an action potential. 2.Hormones: 1. Oxytocin (enhances uterine contractions). 2. Adrenaline (can cause contraction or relaxation of smooth muscle cells). 3.Mechanical Stretch: 1. Stretching the cell mechanically opens calcium channels. 4.Local Factors: 1. Hypoxia, changes in pH, or increased carbon dioxide levels can influence the action potential. Smooth muscle contraction is regulated by the calcium-calmodulin- MLCK pathway, which differs from the troponin-tropomyosin system in skeletal muscle. 1. Contraction begins when an action potential or chemical signal triggers the opening of voltage-gated calcium channels in the sarcolemma 2. Calcium ions (Ca²⁺) flow into the cytoplasm from: The extracellular space. The sarcoplasmic reticulum (via RyR receptors or IP3 receptors). 3. The increased intracellular calcium binds to calmodulin (CaM), a calcium-binding protein. 4. Each calmodulin molecule binds four calcium ions, becoming activated. 5. The calcium-calmodulin complex activates myosin light chain kinase (MLCK), a calcium/calmodulin-dependent enzyme. 6. MLCK phosphorylates the regulatory light chains of myosin molecules, located near the myosin heads. 7. Phosphorylation of the myosin light chain induces a conformational change in myosin, increasing its ATPase activity and enabling it to bind to actin filaments. 8. Phosphorylated myosin heads attach to actin filaments, forming cross-bridges. 9. The myosin heads perform a power stroke, pulling the actin filaments and causing the smooth muscle cell to contract. 10. ATP is hydrolyzed to provide energy for the myosin heads to detach, and reattach to actin, allowing for repeated cycles of contraction. 11. The cycling continues as long as the myosin light chains remain phosphorylated and calcium levels are elevated. Relaxation Relaxation begins when intracellular calcium levels decrease due to: Calcium being pumped back into the sarcoplasmic reticulum via SERCA pumps. Calcium being transported out of the cell via calcium-ATPase pumps or sodium-calcium exchangers. As calcium levels fall, the calcium-calmodulin complex dissociates, inactivating MLCK. Myosin light chain phosphatase (MLCP) dephosphorylates the myosin light chains, reducing the ATPase activity of myosin and stopping the cross-bridge cycling. Latch State (Sustained Contraction) In some cases, smooth muscle can maintain tension (tonic contraction) with minimal ATP consumption through the latch mechanism: Myosin heads remain attached to actin in a dephosphorylated state, maintaining tension without active cycling.