Isoproterenol-mediated parotid gland hypertrophy is inhibited by effectors of 4 beta-galactosyltransferase.

Chronic administration of the beta-adrenergic receptor agonist isoproterenol results in parotid gland hypertrophy and hyperplasia. This physiological change in the gland has recently been reported to be accompanied by a dramatic increase in the rate of synthesis and accumulation of the enzyme 4 beta-galactosyltransferase. Here, isoproterenol-induced hypertrophy of the parotid gland is shown to be blocked by the introduction of the 4 beta-galactosyltransferase modifier protein alpha-lactalbumin and also by specific antiserum to bovine 4 beta-galactosyltransferase. Partial inhibition of gland enlargement was observed stereospecifically with UDP-galactose and with the competitive acceptor glycoprotein, ovalbumin, as well. These agents did not affect the induction by isoproterenol of the biosynthesis of the proline-rich proteins nor of 4 beta-galactosyltransferase. These agents also inhibited the incorporation of thymidine by isoproterenol-stimulated parotid cells in culture.