作者: Peter R. Stanfield
DOI: 10.1007/978-3-642-75636-8_3
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摘要: The discovery in heart muscle of K+ channels closed by the binding ATP (Noma 1983) has its roots an earlier observation that when cells are metabolically exhausted, permeability cell membrane rises substantially. Such a rise was known to occur muscle, where action potential becomes shorter during exhaustion (Trautwein et al. 1954); skeletal resting conductance can increase some 200-fold rigor, resulting inexcitability (Fink and Luttgau 1976); neurones (Godfraind 1970). In most cases initially attributed activation Ca2+-dependent (see for example Krnjevic Lisiewicz 1972), which had already been identified Whittam (1968) red Meech Strumwasser (1970) neurones. Opening such may indeed provide part since ethylene glycol-bis(β-aminoethylether)N,N,N′,N′-tetraacetic acid (EGTA) injection (which will reduce free intracellular Ca2+) reduces change 1983). It is now clear ATP-dependent supply major at least possibly certain as well (Fujiwara 1987; Mourre 1989).