Biomedical Engineering Reference
In-Depth Information
chemical activation with mechanical contraction and relaxation are needed. The
properties of the passive arterial wall have been thoroughly explored both in struc-
tural and mechanical behavior, and there are models available to capture these be-
haviors (Holzapfel et al.,
2000
; Holzapfel and Ogden,
2010
; Schriefl et al.,
2012
).
The properties of the active tone, which mainly originate from the active smooth
muscle, have been less explored in both structure and contractile behavior, and there
is a pressing need for well-defined models of the smooth muscle to better understand
its mechanical properties.
In the following sections the characteristic smooth muscle behavior is described
and followed up with some approaches of modeling smooth muscle contraction and
active tension development. The main part of this chapter reviews and analyzes a
certain mechanochemical modeling approach for smooth muscle (Murtada et al.,
2010a
,
2010b
,
2012
) which is based on structural observations and experimental
data. It is the single model found in the literature which is able to simulate a realistic
behavior of both smooth muscle active tension development at different stretches
and a realistic muscle length behavior during isotonic quick-releases.
4.2 Smooth Muscle Behavior
Smooth muscle behaves differently in both activation and contraction and has a
different underlying structure compared to skeletal and cardiac muscles. Therefore,
it is important, when modeling and studying smooth muscle behavior, to understand
and consider the characteristic behaviors and parameters relevant for smooth muscle
contraction.
4.2.1 Myosin Kinetics
Smooth muscle contraction is regulated through phosphorylation and dephosphory-
lation of the myosin regulatory light-chains (MRLC) which is governed by two main
enzyme activities, the myosin light-chain kinase (MLCK) and the myosin light-
chain phosphatase (MLCP). By changing the membrane potential through depolar-
ization, certain voltage-operated Ca
2
+
channels are opened, allowing an influx of
Ca
2
+
which increases the cytoplasmic calcium. When the cytoplasmic intracellular
calcium increases through an influx of Ca
2
+
from the extracellular matrix, the Ca
2
+
bind to the messenger protein calmodulin (CaM), which activates the MLCK. An al-
ternative way to increase the cytoplasmic intracellular Ca
2
+
is through agonist stim-
ulation, e.g., histamine which attaches to G protein coupled receptors (GPCR) that
activate phospholipase C (PLC) which in turn induces inositol 1,4,5-triphosphate
(InsP
3
) production and Ca
2
+
release from the sarcoplasmic reticulum (SR) (Som-
lyo and Somlyo,
2002
),seealsoFig.
4.1
.
When the myosin is phosphorylated, it can attach to the smooth muscle actin fil-
aments through load-bearing cross-bridges that are able to perform power-strokes
