Mechanism and Control of Saliva Secretion
Nervous regulation of salivary secretions is largely due to parasympathetic stimulation. The salivatory nuclei located near the pons are excited by taste and tactile stimulation in the tongue and mouth. Sour taste stimuli may increase the secretion of saliva to 8 ml/min; tactile stimulation by an object, such as a pipe in the mouth, may also increase the output of saliva. VIP and acetylcholine (ACh), that coexist in parasympathetic nerve endings, cause vasodilation of blood vessels and salivary ducts and stimulate an increase in saliva secretion, respectively. The parasympathetics also stimulate an increase in synthesis and secretion of amylase (ptyalin) and mucus (see top figure). ACh stimulates HCO3- and K+ secretion and absorption of Na+ and Cl- from salivary duct cells. ACh elicits its actions through secondary messengers, inositol triphosphate (IP3)and diacylglycerol (DAG) (see bottom figure). VIP acts via cAMP.
Sympathetic stimulation by norepinephrine can also increase salivary gland secretion, mostly serous, but its effect is short-lived and causes only a slight increase in secretion. This is followed by constriction of blood vessels to the salivary glands and constriction of myoepithelial cells around ducts to ultimately inhibit the secretion of saliva. Various stressful states, like having to speak before a group, can inhibit salivary secretion because the sympathetic system is stimulated. Norepinephrine elicits its action through the secondary messenger cAMP.