We report the influence of adrenergic stimulation on the amplitude and time
course of post-tetanic potentiation of twitch contraction. This was comple
mented by measurements of the peak of [Ca2+](i) transients in twitches and
of the level of myosin light chain 2 (LC2) phosphorylation, before, 20 and
300 s after the conditioning tetanus. Soon after the tetanus, twitch potent
iation and increases of LC2 phosphorylation and of [Ca2+](i) peak were simi
lar in control conditions and in the presence of adrenaline. In control con
ditions, twitch potentiation, LC2 phosphorylation and [Ca2+](i) peak return
ed to, or close to, pre-tetanic values in 300 s. On the contrary, in the pr
esence of adrenaline, twitch potentiation and LC2 phosphorylation were part
ially or fully maintained respectively, while the increase of [Ca2+](i) pea
k was not. This situation allowed us to analyse the relative contributions
of elevated LC2 phosphorylation and [Ca2+](i) peak in the twitch post-tetan
ic potentiation phenomenon. Moreover, it was shown that the increase of LC2
phosphorylation (up to 0.5 mol P/mol LC2) affected neither the kinetic par
ameters of the twitch nor the maximal velocity of shortening. It is propose
d that the maintenance of LC2 phosphorylation in the presence of adrenaline
results from the inhibition of myosin light chain phosphatase. This could
be achieved through the production of the active, phosphorylated form of th
e inhibitor-1, an endogenous inhibitor, which binds to the catalytic sub-un
its common to class 1 protein phosphatases.