Effects of some α‐adrenoceptor stimulating and blocking agents on the salivary amylase secretion in the rabbit

Abstract

In rabbits under urethane anaesthesia parotid secretion of fluid and amylase in response to electrical stimulation of the sympathetic and parasympathetic nerves was measured before and after injections of various agents acting on alpha-adrenoceptors. Amylase secretion in response to sympathetic nerve stimulation at 0.5 and 1 Hz was markedly reduced by clonidine, 0.5-30 micrograms/kg, in a dose related manner. The effect was not due to an altered responsiveness of the gland, since isoprenaline still caused a large release of amylase. Phenylephrine, 10 micrograms/kg, and prazosine, 300 micrograms/kg, had no effect on the sympathetically evoked amylase secretion. Yohimbine in a dose of 0.5 mg/kg increased the amylase output in response to sympathetic nerve stimulation at 0.5 Hz by 70%, while the response at 1 Hz, which is close to maximum for the gland, was not significantly increased. The fluid and amylase secretion produced by parasympathetic nerve stimulation at 1.5, 5.0 and 10 Hz remained unchanged after clonidine, 1.0-30 micrograms/kg, or yohimbine 0.5 mg/kg. In rabbits provided with chronic parotid fistulae fluid and amylase secretion were studied after injections of clonidine, 30 micrograms/kg, and yohimbine, 1 mg/kg. In the conscious animal clonidine reduced not only amylase but also fluid secretion, by around 50 and 30%, respectively, indicating an effect on the activity in both the sympathetic and parasympathetic secretory nerves. Yohimbine increased the output of amylase during feeding, seen as an increased mean output of amylase due to an increased concentration of amylase in the saliva, while fluid secretion remained unchanged. The various experiments suggest that amylase secretion in response to sympathetic activation may be influenced by prejunctional control of transmitter release via alpha-2-adrenoceptors, and that this control may be of physiological significance. Parasympathetically evoked secretion does not seem to be under the influence of a similar control.

Adrenergic Effects on Secretion of Amylase from the Rat Salivary Glands

“…Furthermore, the inhibitory effect of the betai-adrenergic antagonist, atenolol, and the slightly stimulatory effect of the beta2-adrenergic agonist, salbutamol, sug gests that secretion of salivary amylase is predominantly mediated by activation of beta i-adrenergic receptors. These results are in agreement with previous in vivo studies in rabbits demonstrating that salivary secretion of amylase was abolished by betai-adrener gic antagonists as well as clonidine, an alphaadrenergic antagonist [5]. This mode of stim ulation differs from other substances se creted by the salivary glands.…”

Chronic Treatment with Beta Adrenergic Agonists and Antagonists Alters the Composition of Proteins in Rat Parotid Saliva

“…In Study 4, rats received daily intraperitoneal injections of clonidine (at2-adrenergic agonist, 30 ,xg/kg, n = 8; Gjorstrup, 1984), yohimbine (a2-adrenergic antagonist, 1 mg/kg, n = 8; Gjorstrup, 1984), or saline (control, n = 8) for a period of one week. Statistical analysis of the data was performed by means of a t test (Bruning and Kintz, 1977) or analysis of variance (SPSS, Nie et al, 1975).…”

Transdermal neuromodulation of noradrenergic activity suppresses psychophysiological and biochemical stress responses in humans

“…Our physiological and biochemical observations indicate TEN may partially act by producing an increase in α2 adrenergic receptor activity to inhibit NE levels through known negative feedback mechanisms. Clonidine, an α2 adrenoceptor agonist, has been shown to block sAA secretion triggered by sympathetic fiber stimulation 61 . Similarly, we observed that TEN significantly attenuated the levels of sAA following stress induction as discussed above ( Fig.…”