Contraction in smooth muscle starts via phosphorylation of regulatory light chain, i.e. thick filaments.
Ca2+ binds to calmodulin (CM)
Ca2+ CM complex activates myosin light-chain kinase
MLCK activity increases
MLC phosphorylation increases
More cross-bridge cycling = force increases
Ca2+ decreases; MLC phosphatase activity increases relative to MLCK
Relaxation: Ca2+ is removed from the cytosol by…
Ca2+ ATPase on plasma membrane
Ca2+ ATPase on SR membrane (SERCA)
Na+/Ca2+ exchanger on the plasma membrane
Control of smooth muscle Ca2+ influx into the cytosol:
Voltage-gated Ca2+ channels; open due to AP
Stretch-sensitive Ca2+ channels
Chemical messengers interacting with G-protein receptors; open IP3R channels on the SR membrane (no AP needed)
Receptor operated channels; open RyR channels on SR membrane alongside Ca2+ influx from plasma membrane channel (no AP needed)
Pacemaker potentials:
Ca2+ dependent K+ channels close, depolarization to threshold
Voltage-gated Ca2+ channels open, AP occurs
Ca2+ dependent K+ channels open, repolarization
Voltage-gated Ca2+ channels close
The depolarizing phase of a smooth muscle action potential is due to Ca2+ influx through V-gated Ca2+ channels.
Single unit smooth muscle allows a whole tissue to act synchronously, where one input affects all cells in the unit; it contains pacemaker cells, cell connections through gap junctions, and can be initiated by stretch.
Multi unit smooth muscle does not contain pacemaker cells, and activity is usually innervated by second messengers (neurotransmitters or hormones) or by graded potentials.