Volume 49, Issue 3 pp. 806-811
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Synergistic Action of Postsynaptic α-Adrenergic Receptor Stimulation on Vasoactive Intestinal Polypeptide-Induced Increases in Pineal N-Acetyltransferase Activity

A. Yuwiler

Corresponding Author

A. Yuwiler

Neurobiochemistry Research Laboratory, Veterans Administration Medical Center, Brentwood; and Department of Psychiatry and Biobehavioral Sciences, UCLA School of Medicine, University of California, Los Angeles, California, U.S.A.

Address correspondence and reprint requests to Dr. A. Yuwiler at Neurobiochemistry T-85, Veterans Administration Medical Center, Wilshire and Sawtelle Boulevards, Los Angeles, CA 90073, U.S.A.Search for more papers by this author
First published: September 1987
Citations: 20

Abstract

Abstract: The α-adrenergic agonists phenylephrine and methoxamine, at concentrations that have little effect on pineal N-acetyltransferase activity, markedly enhance stimulation of this enzyme by vasoactive intestinal polypeptide (VIP). This augmentation can be blocked by the α1-adrenergic antagonists phenoxybenzamine and prazosin and, at 10 but not 1 μM, by the α2-antagonist yohimbine. The time course for VIP stimulation is not altered by concomitant α-adrenergic stimulation. Augmented activity does not require concomitant α-adrenergic stimulation, but α-adrenergic agonists must be present for augmentation to be maintained. Phorbol 12, 13-diacetate or -dibutyrate but not 4a-phorbol can substitute for phenylephrine, a finding suggesting that protein kinase C is involved in the augmentation. These results are, in general, analogous to α-adrenergic magnification of N-acetyltransferase induction by β-adrenergic agonists.

Abbreviations used:

  • cAMP
  • cyclic AMP
  • ISO
  • L-isoproterenol
  • ME
  • methoxamine
  • NAT
  • serotonin N-acetyltransferase (acetyl-CoA:arylamine N-acetyltransferase
  • EC 2.3.1.5);PE
  • phenylephrine
  • VIP
  • vasoactive intestinal polypeptide
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