Showing papers by "David A. Eisner published in 1988"

Effects of rapid application of caffeine on intracellular calcium concentration in ferret papillary muscles.

Abstract: In this paper we investigate the effects of caffeine (5-20 mM) on ferret papillary muscle. The intracellular Ca2+ concentration ( [Ca2+]i) was measured from the light emitted by the photoprotein aequorin, which had previously been microinjected into superficial cells. Isometric tension was measured simultaneously. The rapid application of caffeine produced a transient increase of [Ca2+]i, which decayed spontaneously within 2-3 s and was accompanied by a transient contracture. The removal of extracellular Na+ or an increase in the concentration of intracellular Na+ (produced by strophanthidin) increased the magnitude of the caffeine response. Cessation of stimulation for several minutes or stimulation at low rates decreased the magnitude of the stimulated twitch and Ca2+ transient. These maneuvers also decreased the size of the caffeine response. These results are consistent with the hypothesis that the caffeine-releasable pool of Ca2+ (sarcoplasmic reticulum) is modulated by maneuvers that affect contraction. Ryanodine (10 microM) decreased the magnitude of the caffeine response as well as that of the stimulated twitch. In contrast, the rapid removal of external Ca2+ abolished the systolic Ca2+ transient within 5 s, but had no effect on the caffeine response. From this we conclude that the abolition of twitch by Ca2+-free solutions is not due to depletion of the sarcoplasmic reticulum of Ca2+, but may be due to a requirement of Ca2+ entry into the cell to trigger Ca2+ release from the sarcoplasmic reticulum.

The effects of nickel on contraction and membrane current in isolated rat myocytes.

Abstract: Depolarization of isolated myocytes for several seconds produces a maintained, tonic component of tension. We have found that this is abolished by 5 mM-Ni2+. Furthermore if Ni2+ is applied after the tonic contraction has developed then its relaxation is prevented. These results are consistent with the hypothesis that Ni2+ inhibits Na+-Ca2+ exchange. Finally, also consistent with an inhibition of Na+-Ca2+ exchange, Ni2+ abolishes the transient inward current while having no effect on the underlying change of [Ca2+]i.