different structure – not striated, elongated, mononuclear, smaller than skeletal (5x20 um)
SR not developed, no T-tubules, filaments not highly ordered, no Z-disk (dense bodies anchor actin)
more actin and tropomyosin relative to myosin but no troponin at all, and lower myosin ATPase activity
(2) Regulation
NO relaxes through cGMP by unknown mechanism
primary regulation still through influx of Ca++, but by three very different mechanisms
(1) neurotrans. or hormone activated Ca++ channels (e.g., purinergic activated by extracell. ATP, a purine)
(2) voltage gated channels – exitation-contraction (e.g., DHP in GI)
(3) G-prot coupled receptors release Ca++ from SR (alpha-andrenergic (epinephrine leads to PLC activation) or angiotensin II)
no depolarization for this one – called pharmomechanical coupling
after contraction, Ca++ pumped back into SR or out of cell
phasic
if relaxes upon Ca++ efflux (GI); tonic if persistant contraction (vascular)
Ca++ regulation different from others – thick filament regulation (also thin filament regulation – passive latch state)
light chain of smooth muscle myosin must be phosphorylated before it will bind actin
calmodulin causes activation of myosin light chain kinase (MLCK)
PKA phosphorylates MLCK, which prevents binding to calmodulin leading to relaxation (MLCP has same effect), so catecholamines lead to smooth muscle relaxation (e.g. epinephrine opens bronchial tubes)
Summary of Muscle Types
– of the three main muscle types (cardiac, skeletal, and smooth):
only cardiac:
cannot recruit more cells to make a stronger contraction (all or none)
cannot produce tetanus (no change in stimulus frequency)
only skeletal:
cannot vary twitch by Ca++ transient
cannot alter Ca++ sensitivity of regulatory systems
only smooth:
can do tonic depolarization (even after intracellular Ca++ has been depleted)
can do pharmomechanical coupling (contraction without depolarization)