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only the initial phase of smooth muscle contraction. Extracellular Ca2+ diffusing into the smooth muscle cell through its plasma membrane is responsible for sustained contractions. This Ca2+ enters primarily through voltage-regulated Ca2+ channels in the plasma membrane. The opening of these channels is graded by the amount of depolarization; the greater the depolarization, the more Ca2+ will enter the cell and the stronger will be the smooth muscle contraction.

The events that follow the entry of Ca2+ into the cytoplasm are somewhat different in smooth muscles than in striated muscles. In striated muscles, Ca2+ combines with troponin. Tro-ponin, however, is not present in smooth muscle cells. In smooth muscles, Ca2+ combines with a protein in the cytoplasm called calmodulin, which is structurally similar to troponin. Calmod-ulin was previously discussed in relation to the function of Ca2+ as a second messenger in hormone action (chapter 11). The calmodulin-Ca2+ complex thus formed combines with and activates myosin light-chain kinase (MLCK), an enzyme that cat-

Chapter Twelve alyzes the phosphorylation (addition of phosphate groups) of myosin light chains, a component of the myosin cross bridges. In smooth muscle (unlike striated muscle), the phosphorylation of myosin cross bridges is the regulatory event that permits them to bind to actin and thereby produce a contraction (fig. 12.34).

Unlike the situation in striated muscle cells, which produce all-or-none action potentials, smooth muscle cells can produce graded depolarizations and contractions without producing action potentials. Indeed, only these graded depolarizations are conducted from cell to cell in many smooth muscles. The greater the depolarization of a smooth muscle cell, the more Ca2+ will enter, and the more MLCK enzymes will be activated. With more MLCK enzymes activated, more cross bridges will become phosphorylated and able to bind to actin. In this way, a stronger depolarization of the smooth muscle cell leads to a stronger contraction.

Relaxation of the smooth muscle follows the closing of the Ca2+ channels and lowering of the cytoplasmic Ca2+ concentrations by the action of Ca2+-ATPase active transport pumps.

AMiAn r»AtAntiilc _

Membrane potential

AMiAn r»AtAntiilc _

Membrane potential

MLCK -(g Inactive

Ca2++ calmodulin

MLCK -(g Inactive

Ca2++ calmodulin

MLCK Active

;Calmodulin-Ca2+ complex

Cross-bridge inactivation and relaxation

Myosin light chain

Myosin light chain

Cross-bridge activation and contraction

Myosin phosphatase

Myosin phosphatase

Figure 12.34 Excitation-contraction coupling in smooth muscle. When Ca2+ passes through voltage-gated channels in the plasma membrane it enters the cytoplasm and binds to calmodulin. The calmodulin-Ca2+ complex then activates myosin light-chain kinase (MLCK) by removing a phosphate group. The activated MLCK, in turn, phosphorylates the myosin light chains, thereby activating the cross bridges to cause contraction. Contraction is ended when myosin phosphatase becomes activated. Upon its activation, myosin phosphatase removes the phosphates from the myosin light chains and thereby inactivates the cross bridges.

Under these conditions, calmodulin dissociates from the myosin light-chain kinase, thereby inactivating this enzyme. The phosphate groups that were added to the myosin are then removed by a different enzyme, a myosin phosphatase (fig. 12.34). Dephos-phorylation inhibits the cross bridge from binding to actin and producing another power stroke.

In addition to being graded, the contractions of smooth muscle cells are slow and sustained. The slowness of contraction is related to the fact that myosin ATPase in smooth muscle is slower in its action (splitting ATP for the cross-bridge cycle) than it is in striated muscle. The sustained nature of smooth muscle contraction is explained by the theory that cross bridges in smooth muscles can enter a latch state.

The latch state allows smooth muscle to maintain its contraction in a very energy-efficient manner, hydrolyzing less ATP than would otherwise be required. This ability is obviously important for smooth muscles, given that they encircle the walls of hollow organs and must sustain contractions for long periods of time. The mechanisms by which the latch state is produced, however, are complex and poorly understood.

The three muscle types—skeletal, cardiac, and smooth— are compared in table 12.9.

Clinical Investigation Clues

Drugs such as nifedipine (Procardia) and related newer compounds are calcium channel blockers. These drugs block Ca2+ channels in the membrane of smooth muscle cells within the walls of blood vessels, causing the muscles to relax and the vessels to dilate. This effect, called vasodilation, may be helpful in treating some cases of hypertension (high blood pressure). Calcium-channel-blocking drugs are also used when spasm of the coronary arteries (vasospasm) produces angina pectoris, which is pain caused by insufficient blood flow to the heart.

Remember that Maria was taking a calcium-channel-blocking drug to treat her hypertension.

How do such drugs help to lower blood pressure?

Is it likely that this drug contributed to Maria's skeletal muscle pain and fatigue?

Could it raise her blood Ca2+ levels? If not, what could raise her blood Ca2+?

Single-Unit and Multiunit Smooth Muscles Smooth muscles are often grouped into two functional categories: single-unit and multiunit (fig. 12.35). Single-unit smooth muscles have numerous gap junctions (electrical synapses) between adjacent cells that weld them together electrically; they thus behave as a single unit, much like cardiac muscle. Most smooth muscles—including those in the digestive tract and uterus—are single-unit.

Only some cells of single-unit smooth muscles receive au-tonomic innervation, but the ACh released by the axon can diffuse to other smooth muscle cells. Binding of ACh to its muscarinic receptors causes depolarization by closing K+ channels, as described in chapter 9 (see fig. 9.11). Such stimulation, however, only modifies the automatic behavior of single-unit smooth muscles. Single-unit smooth muscles display pacemaker activity, in which certain cells stimulate others in the mass. This is similar to the situation in cardiac muscle. Single-unit smooth muscles also display intrinsic, or myogenic, electrical activity and contraction in response to stretch. For example, the stretch induced by an increase in the volume of a ureter or a section of the digestive tract can stimulate myogenic contraction. Such contraction does not require stimulation by autonomic nerves.

Contraction of multiunit smooth muscles, by contrast, requires nerve stimulation. Multiunit smooth muscles have few, if

Table 12.9 Comparison of Skeletal, Cardiac, and Smooth Muscle

Skeletal Muscle

Cardiac Muscle

Smooth Muscle

Striated; actin and myosin arranged in sarcomeres

Striated; actin and myosin arranged in sarcomeres

Not striated; more actin than myosin; actin inserts into dense bodies and cell membrane

Well-developed sarcoplasmic reticulum and transverse tubules

Moderately developed sarcoplasmic reticulum and transverse tubules

Poorly developed sarcoplasmic reticulum; no transverse tubules

Contains troponin in the thin filaments

Contains troponin in the thin filaments

Contains calmodulin, a protein that, when bound to Ca2+, activates the enzyme myosin light-chain kinase

Ca2+ released into cytoplasm from sarcoplasmic reticulum

Ca2+ enters cytoplasm from sarcoplasmic reticulum and extracellular fluid

Ca2+ enters cytoplasm from extracellular fluid, sarcoplasmic reticulum, and perhaps mitochondria

Cannot contract without nerve stimulation; denervation results in muscle atrophy

Can contract without nerve stimulation; action potentials originate in pacemaker cells of heart

Maintains tone in absence of nerve stimulation; visceral smooth muscle produces pacemaker potentials; denervation results in hypersensitivity to stimulation

Muscle fibers stimulated independently; no gap junctions

Gap junctions present as intercalated discs

Gap junctions generally present

Fox: Human Physiology, Eighth Edition

12. Muscle: Mechanisms of Contraction and Neural Control

Text

© The McGraw-H Companies, 2003

Chapter Twelve

Autonomic neuron

Synapses en passant

Smooth muscle cell

Gap junctions

Autonomic neuron

Synapses en passant

Figure 12.35 Single-unit and multiunit smooth muscle. In single-unit smooth muscle, the individual smooth muscle cells are electrically joined by gap junctions, so that depolarizations can spread from one cell to the next. In multiunit smooth muscle, each smooth muscle cell must be stimulated by an axon. The axons of autonomic neurons have varicosities, which release neurotransmitters, and which form synapses en passant with the smooth muscle cells.

Autonomic neuron

Synapses en passant

Smooth muscle cell

Gap junctions

Autonomic neuron

Synapses en passant

Figure 12.35 Single-unit and multiunit smooth muscle. In single-unit smooth muscle, the individual smooth muscle cells are electrically joined by gap junctions, so that depolarizations can spread from one cell to the next. In multiunit smooth muscle, each smooth muscle cell must be stimulated by an axon. The axons of autonomic neurons have varicosities, which release neurotransmitters, and which form synapses en passant with the smooth muscle cells.

any, gap junctions. The cells must thus be stimulated individually by nerve fibers. Examples of multiunit smooth muscles are the arrector pili muscles in the skin and the ciliary muscles attached to the lens of the eye.

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