Key result
Isoproterenol treatment of rat ventricular trabeculae increased Ca2+ release from the sarcoplasmic reticulum in response to trigger Ca2+, likely due to phosphorylation of the Ca2+ release channel.
Why the study?
Does isoproterenol treatment increase Ca2+ release from the sarcoplasmic reticulum in rat ventricular trabeculae?
Does isoproterenol treatment increase Ca2+ release from the sarcoplasmic reticulum in rat ventricular trabeculae?
Phosphorylation of sarcoplasmic reticulum proteins, likely the Ca2+ release channel, increases Ca2+ release in response to trigger Ca2+ in rat ventricular trabeculae.
Hypothesis-generating for beta-adrenergic Ca2+ handling in rodents; should not yet change clinical practice.
Effects on Ca(2+)-induced Ca2+ release due to phosphorylation of sarcoplasmic reticulum (SR) proteins were investigated in isoproterenol-treated saponin-permeabilized trabeculae from rat ventricles. In these experiments, Ca2+ release from the SR was induced by a rapid change in concentration of free Ca2+ (ie, trigger Ca2+) achieved by flash photolysis of nitr-5, and the amount of Ca2+ released was assessed by measuring isometric tension. Ca2+ uptake by the SR was more rapid, and the amount of Ca2+ released by a given concentration of trigger Ca2+ was greater in isoproterenol-treated trabeculae compared with control trabeculae. However, under the same conditions of Ca2+ loading, the amplitudes of caffeine-elicited tension transients in control trabeculae were similar to those in isoproterenol-treated trabeculae, suggesting that the Ca2+ available for release was similar in the two cases. Control experiments showed that there were no significant differences in Ca2+ sensitivity of tension between isoproterenol-treated and control trabeculae. Also, application of alkaline phosphatase to trabeculae that had previously been treated with isoproterenol returned SR Ca2+ release to control levels. We conclude that the greater release of Ca2+ in isoproterenol-treated trabeculae in response to a given concentration of trigger Ca2+ is due to phosphorylation of SR proteins, most likely the Ca2+ release channel.
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Patel et al. (1995) studied this question. Isoproterenol treatment vs. Control trabeculae was evaluated on Amount of Ca2+ released assessed by measuring isometric tension. Isoproterenol treatment of rat ventricular trabeculae increased Ca2+ release from the sarcoplasmic reticulum in response to trigger Ca2+, likely due to phosphorylation of the Ca2+ release channel.
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