By Linda S. Costanzo PhD
- NEW! Full-color layout, movement charts, illustrations, and tables that summarize info for handy review
- Each bankruptcy is written within the well known Board evaluation Series (BRS) define layout and contours bolded keyword phrases to streamline your study
- Over 350 USMLE-style questions, solutions, and rationales either electronically and in print make stronger your body structure review
- A FREE significant other web site deals a web booklet and an interactive query financial institution with the entire questions from the booklet so that you can customise your assessment tests!
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Extra info for BRS Physiology
Are present in the I bands. interdigitate with the thick filaments in a portion of the A band. contain actin, tropomyosin, and troponin. a. Troponin is the regulatory protein that permits cross-bridge formation when it binds Ca2+. b. Troponin is a complex of three globular proteins: ■ ■ ■ Troponin T (“T” for tropomyosin) attaches the troponin complex to tropomyosin. Troponin I (“I” for inhibition) inhibits the interaction of actin and myosin. Troponin C (“C” for Ca2+) is the Ca2+-binding protein that, when bound to Ca2+, permits the interaction of actin and myosin.
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. t a b l e 1-3 Comparison of Skeletal, Smooth, and Cardiac Muscle Feature Skeletal Muscle Smooth Muscle Cardiac Muscle Appearance Upstroke of action potential Striated Inward Na+ current No striations Inward Ca2+ current Plateau No No Duration of action potential ~1 msec ~10 msec Excitation–contraction coupling Action potential → T tubules Action potential opens voltage-gated Ca2+ channels in cell membrane Striated Inward Ca2+ current (SA node) Inward Na+ current (atria, ventricles, Purkinje fibers) No (SA node) Yes (atria, ventricles, Purkinje fibers; due to inward Ca2+ current) 150 msec (SA node, atria) 250–300 msec (ventricles and Purkinje fibers) Inward Ca2+ current during plateau of action potential Ca2+ released from nearby SR ↑ [Ca2+]i Molecular basis for contraction Ca2+–troponin C Ca2+-induced Ca2+ release from SR Hormones and transmitters open IP3 – gated Ca2+ channels in SR ↑ [Ca2+]i Ca2+–calmodulin ↑ myosin light-chain kinase Ca2+–troponin C IP3 = inositol 1,4,5-triphosphate; SA = sinoatrial; SR = sarcoplasmic reticulum.
As long as intracellular Ca2+ concentration is low, cross-bridge cycling cannot occur. 6. Mechanism of tetanus. A single action potential causes the release of a standard amount of Ca2+ from the SR and produces a single twitch. However, if the muscle is stimulated repeatedly, more Ca2+ is released from the SR and there is a cumulative increase in intracellular [Ca2+], extending the time for cross-bridge cycling. The muscle does not relax (tetanus). C. Length–tension and force–velocity relationships in muscle ■ ■ Isometric contractions are measured when length is held constant.
BRS Physiology by Linda S. Costanzo PhD