Synergistic Action of Postsynaptic α-Adrenergic Receptor Stimulation on Vasoactive Intestinal Polypeptide-Induced Increases in Pineal N-Acetyltransferase Activity
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