Smooth Muscle Contraction and Relaxation

Overview

Neuromuscular Junction: Action potential arrives, acetylcholine released.
Muscle Membrane: Acetylcholine binds, sodium enters, End Plate Potential (threshold reached).
Action Potential: Propagation along membrane and into T-tubules.
Surface Reaction: Dihydropyridine Receptor (calcium channel) activates Ryanodine Receptor (sarcoplasmic reticulum surface).
Calcium Release: Calcium exits sarcoplasmic reticulum, binds to Troponin C.
Contraction: Troponin C moves tropomyosin, myosin binds to actin, ATPase activity in myosin head bends, thin filament slides, sarcomere shortens.
Relaxation: Calcium ATPase pumps calcium back, muscle relaxes as calcium levels drop.

Calcium Requirement: Intracellular calcium level rise necessary for contraction; sources differ from skeletal muscle.
Voltage-Dependent Pathways: Action potentials driven more by calcium entry than sodium in smooth muscle.
Resting Membrane Potential: Variable in smooth muscle; features spike potentials and plateaus (slow calcium channel closure).
Single vs. Multi-Unit: Single-unit (action potentials, self-generating waves) vs. multi-unit (independent cells, junctional potentials).

Slow Wave Rhythm: Self-generated in single-unit muscles, isn’t strong enough alone—requires reaching threshold for action potentials.
Local Factors: Oxygen, carbon dioxide, hydrogen ion levels influence contraction (e.g., blood vessel dilation/constriction).
Hormonal Factors: Hormones acting on ligand-gated calcium channels, activating second messengers (e.g., phospholipase C producing IP3).
Calcium-Induced Calcium Release: IP3 important, extracellular fluid primary source of calcium.

Different Proteins: No troponin, uses calmodulin instead.
Calcium-Calmodulin Complex: Forms, activates protein kinase, phosphorylates Calponin (removes myosin ATPase inhibition), activates myosin light chain kinase (MLCK).
Phosphorylation: Myosin needs phosphorylation for ATPase activity—essential for cross-bridge cycling.

Calcium Removal: ATPase pumps and sodium-calcium exchangers reduce intracellular calcium.
Dephosphorylation: Myosin light chain phosphatase removes phosphate—stopping contraction.

Latch-Bridge Phenomenon: Sustain contraction without ATP use (slow actin-myosin cycling).
Stress-Relaxation: Adaptation to stretch, e.g., bladder expansion.
Regulatory Factors: Neural, hormonal, neurotransmitters, local factors determine contraction/relaxation state.
Calcium-Independent Mechanisms: Involves myosin light chain phosphorylation/dephosphorylation.

Smooth muscle shows unique mechanisms for contraction/relaxation, responding to various stimuli involuntarily.
Importance of calcium and regulatory pathways highlighted.

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