Adrenergic Effects on Secretion of Amylase from the Rat Salivary Glands

Abstract

The present study was undertaken to investigate the effect of adrenergic agents on secretion of amylase from the salivary glands in vivo. Saliva was collected from the distal oesophagus in conscious rats. Adrenaline increased the concentration of amylase in saliva and serum significantly. The result of infusion of alpha- and beta-adrenergic antagonists as well as noradrenaline and isoproterenol showed that secretion of salivary amylase is predominantly mediated by stimulation of beta-adrenergic receptors, especially of the beta₁-subtype. Investigation of the isoenzyme pattern in saliva, pancreatic juice and serum demonstrated that the major component in serum is salivary amylase. This study has shown that beta-adrenergic agents stimulate secretion of amylase from the salivary glands in rats. Though the secretion is mainly exocrine small amounts of amylase is found in serum, which seems to originate from the salivary glands.

Norepinephrine infusion with and without alpha-adrenergic blockade by phentolamine increases salivary alpha amylase in healthy men

“…Compared to control rats receiving saline-infusion only, NEbut also EPI-infusion elicited significantly higher sAA levels (Skov Olsen et al, 1988). With respect to observed associations between stress-induced NE and sAA release, results of that animal study may be interpreted in that stress-induced NE increases mediate (at least in part) sAA release (Skov Olsen et al, 1988). While in humans, a direct effect of NEor EPI-infusion on sAA has not yet been investigated, studies using the non-selective beta-adrenergic agonist isoprenaline similarly observed a rise in sAA levels following isoprenaline infusion (Katz and Mandel, 1968;Speirs et al, 1974).…”

“…To date, the role of alpha-adrenergic receptors in mediation of stress-induced sAA increases is still unclear. In the previously mentioned pioneer infusion study in rats blockade of alpha1-and alpha2-adrenergic receptors by phenoxybenzamine reduced EPI-infusion-induced sAA increases (Skov Olsen et al, 1988). Notably, in that study blockade of alpha-adrenergic receptors was associated with lower inhibition of EPI-infusion induced sAA release as compared to non-selective beta-adrenergic blockade by propranolol (Skov Olsen et al, 1988).…”

“…Saliva was collected over several hours and sAA levels were assessed. Compared to control rats receiving saline-infusion only, NEbut also EPI-infusion elicited significantly higher sAA levels (Skov Olsen et al, 1988). With respect to observed associations between stress-induced NE and sAA release, results of that animal study may be interpreted in that stress-induced NE increases mediate (at least in part) sAA release (Skov Olsen et al, 1988).…”

“…In the previously mentioned pioneer infusion study in rats blockade of alpha1-and alpha2-adrenergic receptors by phenoxybenzamine reduced EPI-infusion-induced sAA increases (Skov Olsen et al, 1988). Notably, in that study blockade of alpha-adrenergic receptors was associated with lower inhibition of EPI-infusion induced sAA release as compared to non-selective beta-adrenergic blockade by propranolol (Skov Olsen et al, 1988). In contrast, two human studies suggest stimulatory effects of alpha adrenergic blockade on sAA: in 5 men higher sAA increases had been observed following isoprenaline-infusion after alpha1-and alpha2adrenergic receptor blockade by phentolamine (Katz and Mandel, 1968).…”

“…To date, the effect of NE-infusion on sAA release has been investigated in one animal study (Skov Olsen et al, 1988). In that pioneer study NE but also EPI were infused in 8 rats over a period of 3 h in supraphysiological dosage.…”