Файл: BRS_Physiology_6E_2014_1.pdf

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Figure 1.12 Cross-bridge cycle. Myosin “walks” toward the plus end of actin to produce shortening and force generation. ADP = adenosine diphosphate; ATP = adenosine triphosphate; Pi = inorganic phosphate.

C.Length–tension and force–velocity relationships in muscle

■Isometric contractions are measured when length is held constant. Muscle length (preload) is

fixed, the muscle is stimulated to contract, and the developed tension is measured. There is no shortening.

■Isotonic contractions are measured when load is held constant. The load against which the muscle contracts (afterload) is fixed, the muscle is stimulated to contract, and shortening is measured.

1.  Length–tension relationship (Figure 1.14)

■measures tension developed during isometric contractions when the muscle is set to fixed lengths (preload).

■has little or no electrical coupling between cells.

■is densely innervated; contraction is controlled by neural innervation (e.g., autonomic nervous system).

2.  Unitary (single-unit) smooth muscle

■is the most common type and is present in the uterus, gastrointestinal tract, ureter, and bladder.

■is spontaneously active (exhibits slow waves) and exhibits “pacemaker” activity (see Chapter 6 III A), which is modulated by hormones and neurotransmitters.

■has a high degree of electrical coupling between cells and, therefore, permits coordinated contraction of the organ (e.g., bladder).

3.  Vascular smooth muscle

■has properties of both multiunit and single-unit smooth muscle.

B. Steps in excitation–contraction coupling in smooth muscle (Figure 1.16)

■The mechanism of excitation–contraction coupling is different from that in skeletal muscle.

■There is no troponin; instead, Ca2+ regulates myosin on the thick filaments.

22brs Physiology

1.Depolarization of the cell membrane opens voltage-gated Ca2+ channels and Ca2+

flows into the cell down its electrochemical gradient, increasing the intracellular [Ca2+]. Hormones and neurotransmitters may open ligand-gated Ca2+ channels in the cell membrane. Ca2+ entering the cell causes release of more Ca2+ from the SR in

a process called Ca2+-induced Ca2+ release. Hormones and neurotransmitters also directly release Ca2+ from the SR through inositol 1,4,5-trisphosphate (IP3)–gated Ca2+ channels.

2.Intracellular [Ca2+] increases.

3.Ca2+ binds to calmodulin. The Ca2+–calmodulin complex binds to and activates myosin light chain kinase. When activated, myosin light chain kinase phosphorylates myosin and

allows it to bind to actin, thus initiating cross-bridge cycling. The amount of tension produced is proportional to the intracellular Ca2+ concentration.

4.A decrease in intracellular [Ca2+] produces relaxation.

VIII. CoMParIson oF sKeleTal MusCle, sMooTH MusCle,

anD CarDIaC MusCle

■Table 1.3 compares the ionic basis for the action potential and mechanism of contraction in skeletal muscle, smooth muscle, and cardiac muscle.

■Cardiac muscle is discussed in Chapter 3.

Purkinje fibers; due to inward Ca2+ current)

IP3 = inositol 1,4,5-triphosphate; SA = sinoatrial; SR = sarcoplasmic reticulum.