A comparison of the effects of UTP and ATP on the Ca2+ release channel of skeletal muscle sarcoplasmic reticulum.
Heavy sarcoplasmic reticulum (SR) membrane fractions from rabbit and porcine skeletal muscle were incorporated into planar lipid bilayers and the activity of the Ca2+ release channels was recorded under voltage clamp, using Cs+ as the current carrier. The effects of the nucleotides adenosine triphosphate (ATP) and uridine triphosphate (UTP) on channel activity were studied at a holding potential of +30 mV. UTP (0.1-1.0 mM) had no effect per se on the conductance or the gating properties of the Ca2+ release channels. In contrast, ATP (> 0.1 mM) increased P(o), the open channel probability, and both tau o1 and tau o2, the open time constants, and decreased tau c1 and tau c2, the closed time constants. The Ca2+ channel conductance, however, was not affected by ATP. Ruthenium red (1-2 microM), a well-known inhibitor of the SR Ca2+ release channel, abolished the ATP-induced channel activation. These electrophysiological data provide support for our contention (G. Suarez-Kurtz et al. (1993). Anais da Academia Brasileira de Ciências, 65:330) that the UTP-induced tension in mammalian "skinned" muscle fibers is not due to stimulated release of SR-stored Ca2+ via the release channel.
Suarez-Kurtz
G
G
Departamento de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Brasil.
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D015220:Calcium Channels / Q000187:drug effects* / Q000378:metabolism; D004594:Electrophysiology; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism; D011817:Rabbits; D012519:Sarcoplasmic Reticulum / Q000378:metabolism*; D013552:Swine; D014544:Uridine Triphosphate / Q000494:pharmacology*
D015220:Calcium Channels; D000255:Adenosine Triphosphate; D014544:Uridine Triphosphate