CHAPTER 3 • CELLULAR STRUCTURE AND FUNCTION
51
Dense
Enlarged cross-section
of actin and myosin
■ FIGURE 3.8 Vascular sm ooth muscle cell structure. Actin and myosin filaments are connected by dense
bodies and dense bands. Each myosin filam ent is surrounded by several actin filaments. N, nucleus.
surrounded by several actin filaments. Similar
to cardiac myocytes, vascular smooth muscle
cells are electrically connected by gap junc-
tions. These low-resistance intercellular con-
nections allow propagated responses along the
length of the blood vessels. For example, elec-
trical depolarization and contraction of a local
site on an arteriole can result in depolarization
at a distant site along the same vessel, indicat-
ing cell-to-cell propagation of the depolarizing
currents.
VASCULAR SMOOTH MUSCLE
CONTRACTION
Contractile characteristics and the mecha-
nisms
responsible
for
contraction
differ
considerably between vascular smooth mus-
cle and cardiac myocytes. Vascular smooth
muscle tonic contractions are slow and sus-
tained, whereas cardiac muscle contractions
are rapid and relatively short (a few hundred
milliseconds). In blood vessels, the smooth
muscle is normally in a partially contracted
state, which determines the resting tone or
diameter of the vessel. This tonic contraction
is determined by stimulatory and inhibitory
influences acting on the vessel. As described
in later chapters, the most important of these
are sympathetic adrenergic nerves, circulating
hormones (e.g., epinephrine, angiotensin II),
substances released by the endothelium lining
the vessel, and vasoactive substances released
by the tissue surrounding the blood vessel.
Vascular
smooth
muscle
contraction
can be initiated by electrical, chemical, and
mechanical stimuli. Electrical depolarization
of the vascular smooth muscle cell membrane
using electrical stimulation elicits contraction
primarily
by
opening
voltage-dependent
calcium channels (L-type calcium channels),
which causes an increase in the intracellular
concentration of calcium. Membrane depolar-
ization can also occur through changes in ion
concentrations (e.g., depolarization induced
by high concentrations of extracellular potas-
sium) or by the receptor-coupled opening of
ion channels, particularly calcium channels.
Many different chemical stimuli, such as
norepinephrine, epinephrine, angiotensin II,
vasopressin, endothelin-1, and thromboxane A2
can elicit contraction. Each of these substances
binds to specific receptors on the vascular
smooth muscle cell. Different signal transduc-
tion pathways converge to increase intracellu-
lar calcium, thereby eliciting contraction.
Mechanical stimuli in the form of passive
stretching of smooth muscle in some arter-
ies can cause a contraction that originates
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