Dual adrenergic control of in vivo choline levels in the mouse major salivary glands

Summary 1 The purpose of this study was to demonstrate that the adrenergic nervous system regulates the in vivo choline levels in the mouse major salivary glands. 2 Methoxamine (α1-adrenoceptor agonist, 2.5–20 mg kg−1, s.c.) elevated choline levels dose-dependently and the effect of methoxamine (10 mg kg−1) was completely inhibited by the α-adrenoceptor antagonist phentolamine (5 mg kg−1, i.p.) but not by the β-adrenoceptor antagonist propranolol (3 mg kg−1, i.p.). 3 In contrast, isoprenaline (β-adrenoceptor agonist 0.25–20 mg kg−1, s.c.) lowered choline levels and the effect of isoprenaline (2 mg kg−1) was inhibited by propranolol, but not by phentolamine. 4 Noradrenaline (1–4 mg kg−1, s.c.) manifested both the α- and β-adrenergic actions depending on its dose. Noradrenaline at 1–2 mg kg−1, lowered choline levels and the effect of noradrenaline (1 mg kg−1) was inhibited by propranolol, but not by phentolamine. On the other hand, noradrenaline (4 mg kg−1) elevated choline levels and the effect was blocked by phentolamine, but not by propranolol. 5 Tyramine (5–80 mg kg−1, s.c.) elicited the release of noradrenaline from sympathetic nerve terminals and induced essentially the same effects on the choline levels as noradrenaline. Tyramine (10 mg kg−1) lowered choline levels and the effect was inhibited by propranolol, but not by phentolamine. However, tyramine (80 mg kg−1) elevated choline levels and the effect was inhibited by phentolamine, but not by propranolol. 6 These results suggest that choline levels in the salivary glands may be under separate α- and β-adrenergic control and suggest a possibility that the neurotransmitter noradrenaline released for sympathetic nerve terminals can manage the dual control of choline levels in some autonomic organs in a characteristic dose-dependent manner.