| Popis: |
Publisher Summary In this chapter the results of the experiments using Ni2+ suggest that, in heart muscle beating at close to physiological rates, the inhibition of transsarcolemmal Ca2+ influx inhibits Ca2+-induced release of sarcoplasmic reticular (SR) Ca2+ without decreasing the amount of Ca2+ stored in the SR. Moreover, the negative inotropic effect arising solely from the inhibition of the transsarcolemmal Ca2+ influx is rather small for contractions that are largely dependent on SR Ca2+. The model in which SR Ca2+ release is regulated by the product of the transsarcolemmal Ca2+ influx and the amount of releasable SR Ca2+ may account for the difference in the effects of an inhibitor of the Ca2+ influx on the force of the steady-state contraction and that of the postrest contraction. Even if the total SR Ca2+ content is the same in the two types of contractions, the amount of releasable SR Ca2+ is most likely smaller in the steady-state contraction at a high frequency than in the postrest contraction owing to the time-dependent process by which SR Ca2+ becomes available for release. The proposed model predicts that the larger the amount of releasable SR Ca2+, the smaller is the transsarcolemmal Ca2+ influx required for the same amount of SR Ca2+ release. Although the effects of thiopental and Ni2+ have been similar, the anesthetic differed from Ni2+ with respect to relative effect on the postrest contraction compared at the same level of inhibition of the transsarcolemmal Ca2+ influx and with respect to its effect on the postrest contraction measured in the presence of ryanodine. Thus, thiopental appears to have a direct effect on the SR Ca2+ release mechanism in such a way that SR Ca2+ release is inhibited whether the release is triggered by the transsarcolemmal Ca2+ influx or by the action of ryanodine. |
