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In the first 24 h after a single injection of the β-adrenergic agonist isoprenaline to mice, the level of β-actin mRNA in the parotid glands increased significantly above that observed in untreated mice. The increase was transient, reaching 11 times the normal level 18 h after treatment and declining thereafter. Repeated daily doses of isoprenaline did not result in any further increase in β-actin mRNA. Nuclear transcription experiments showed that there was no increase in the transcription rate of the β-actin gene 8 h after an injection of isoprenaline, although β-actin mRNA levels were increasing at this time. Immunoblotting revealed an increase in β-actin protein in parotid gland samples after isoprenaline treatment, although the increase was not to the same extent as the mRNA, perhaps indicating that degradation of β-actin had also increased. Using immunocytochemistry it was found that β-actin was located mainly in the apical cortex of the normal acinar cell. There was a significant decrease in cortical β-actin 24 h after isoprenaline treatment, suggesting that the β-actin was under the process of redistribution.

From these data we propose that isoprenaline caused an increase in β-actin synthesis by a post-transcriptional mechanism and a redistribution of β-actin in preparation for the well-known subsequent change in morphology and function of the parotid glands.