excitation-contraction coupling


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excitation-contraction coupling

the link between excitation of muscle membrane and initiation of force generation at cross-bridges, producing muscle contraction. In all types of muscle this involves a rise in cytoplasmic calcium concentration [Ca2+] but mechanisms for this rise differ substantially. In healthy skeletal muscle the sarcoplasmic reticulum (SR) is the sole effective source of Ca2+ which (within normal physiological function) can only be released from the SR by a muscle action potential (AP), triggered via the motor nerve. In cardiac muscle, the AP is spontaneously initiated in cardiac pacemaker cells rather than by nerves, and Ca2+ release from the SR is triggered by Ca2+ itself, entering the cell from the extracellular fluid during the AP. In certain smooth muscle masses, neural control mechanisms analogous to those of skeletal muscle operate but more commonly, hormones and/or other chemicals are involved; the Ca2+ comes from both the SR and the extracellular fluid, as it does in cardiac muscle, but mediated largely by different mechanisms.

excitation

an act of irritation or stimulation; a condition of being excited or of responding to a stimulus; the addition of energy, as the excitation of a molecule by absorption of photons.

excitation-conduction-contraction
in the stimulation of muscle contraction this is the coupling which occurs at the sarcolemma-sarcoplasmic reticulum junction. Mediated by the release of calcium ions in the aqueous sarcoplasm.
excitation-contraction coupling
conversion of an excitation stimulus into contraction of the effector muscle fiber; ionic calcium is the link between the two.
indirect excitation
electrostimulation of a muscle by placing the electrode on its nerve.
excitation-secretion
in the stimulation of muscular contraction this is the stimulation of secretion of acetylcholine from the vesicles in the cholinergic nerve terminals into the synaptic cleft at the nerve-muscle junction.
excitation signs
see irritation nervous signs.
References in periodicals archive ?
These are the presence of disrupted force-bearing structures and damage to excitation-contraction coupling system (Proske and Allen, 2005; Warren et al.
1:30 "Characterization of excitation-contraction coupling in diabetic hypertensive cardiomyopathy in adult rat ventricular myocytes," Loren Wold *, David Relling, and Jun Ren, Department of Pharmacology, Physiology & Therapeutics, University of North Dakota, Grand Forks.