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In epithelial cells of the excretory and striated ducts, the simplified model of ion transport processes is shown in Fig. 28.4. The electrochemical gradients for Na+ and K+ that drive most of the other ionic transport processes of the cell are maintained by Na+,K+-ATPase located in the basolateral membrane. In the apical membrane, the absorption of Na+ and Cl- from the lumen and the secretion of K+ and HCO3- into the lumen are the result of the parallel operation of the Na+/ H+ antiporter, the Cl-/HCO3- antiporter, and the H+/K+ antiporter. The ductular epithelium is relatively impermeable to water, preventing excessive water absorption by osmosis.
Fig. 28.3 depicts the ionic transport mechanism involved in the secretion of amylase and electrolytes in salivary acinar cells. The swallowing reflex, which is almost entirely under reflex control after being voluntarily initiated, is a rigidly ordered sequence of events that propels food from the mouth to the pharynx and then to the stomach. This reflex also inhibits respiration and prevents food from entering the trachea during swallowing. Stimulation of touch receptors, particularly those near the opening of the pharynx, initiates the afferent limb of the swallowing reflex. Sensory impulses from these receptors are transmitted to the swallowing center located in the medulla and lower pons. Motor impulses from the swallowing center travel via various cranial nerves to the musculature of the pharynx and upper esophagus, and to the remainder of the esophagus through vagal motor neurons.
The timing of events in swallowing is illustrated in Fig. 28.5. The voluntary phase of swallowing is initiated by the separation of a bolus of food from the mass of food in the mouth by the tip of the tongue. The bolus is then moved upward and backward into the mouth by the action of the tongue, pressing against the hard palate. Subsequently, the bolus is forced into the pharynx, stimulating the touch receptors.
Fig. 28.4 demonstrates the ionic transport mechanism involved in secretion and absorption in epithelial cells of the striated and excretory duct of the salivary gland. The release of acetylcholine, norepinephrine, substance P, and VIP by salivary glands is stimulated by nerves, resulting in increased secretion of amylase and saliva flow. These neurotransmitters primarily increase the intracellular concentration of cyclic adenosine monophosphate (cAMP) and Ca++ in the cytosol. Muscarinic and tachykinin receptors, activated by acetylcholine and substance P, respectively, elevate the cytosolic concentration of Ca++ in serous acinar cells. On the other hand, norepinephrine, acting on β receptors, and VIP, binding to its receptor, elevate the cAMP concentration in acinar cells. Agonists that elevate the cAMP concentration in serous acinar cells induce a secretion rich in amylase, while those that mobilize Ca++ elicit a more voluminous secretion with a lower concentration of amylase. Ca++-mobilizing agonists may also increase the concentration of cyclic guanosine monophosphate (cGMP), which may mediate the trophic effects caused by these agonists.

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Fig. 28.4 shows a simplified model of ion transport processes in epithelial cells of the excretory and striated ducts. Na+,K+-ATPase located in the basolateral membrane maintains the electrochemical gradients for Na+ and K+ that drive most of the other ionic transport processes of the cell. In the apical membrane the parallel operation of the Na+/ H+ antiporter, the Cl−/HCO3 − antiporter, and the H+/K+ antiporter results in absorption of Na+ and Cl− from the lumen and secretion of K+ and HCO3 − into the lumen. The relative impermeability of the ductular epithelium to water prevents the ducts from absorbing too much water by osmosis.
• Fig.28.3Ionic transport mechanism involved in the secretion of amylase and electrolytes in salivary acinar cells. ATP2Cl–HCO3LumenofacinusNa˜Na˜Na˜Cl°Na˜K˜K˜K˜K˜°H˜
Swallowing can be initiated voluntarily, but thereafter it is almost entirely under reflex control. The swallowing reflex is a rigidly ordered sequence of events that propel food from the mouth to the pharynx and from there to the stomach. This reflex also inhibits respiration and prevents entrance of food into the trachea during swallowing. The afferent limb of the swallowing reflex begins when touch receptors, most notably those near the opening of the pharynx, are stimulated. Sensory impulses from these receptors are transmitted to an area in the medulla and lower pons called the swallowing center. Motor impulses travel from the swallowing center to the musculature of the pharynx and upper esophagus via various cranial nerves and to the remainder of the esophagus by vagal motor neurons.
The timing of events in swallowing is shown in
Fig. 28.5 . The voluntary phase of swallowing is initiated when the tip of the tongue separates a bolus of food from the mass of food in the mouth. First the tip of the tongue and later the more posterior portions of the tongue press against the hard palate. The action of the tongue moves the bolus upward and then backward into the mouth. The bolus is forced into the pharynx, where it stimulates the touch receptors
CHAPTER 28 The Cephalic, Oral, and Esophageal Phases of the Integrated Response to a Meal • Fig.28.4Ionic transport mechanism involved in secretion and absorption in epithelial cells of the striated and excretory duct of the salivary gland. ATPHCO3LumenofductNa˜Na˜Na˜Na˜Cl°Cl°K˜K˜K˜°H˜H˜H˜
The acinar cells and duct cells of the salivary glands respond to both cholinergic and adrenergic agonists. Nerves stimulate the release of acetylcholine, norepinephrine, substance P, and VIP by salivary glands, and these hormones increase the secretion of amylase and the flow of saliva. These neurotransmitters act mainly by elevating the intracellular concentration of cyclic adenosine monophosphate (cAMP) and by increasing the concentration of Ca++ in the cytosol. Acetylcholine and substance P, acting on muscarinic and tachykinin receptors, respectively, increase the cytosolic concentration of Ca++ in serous acinar cells. In contrast, norepinephrine, acting on β receptors, and VIP, binding to its receptor, elevate the cAMP concentration in acinar cells. Agonists that elevate the cAMP concentration in serous acinar cells elicit a secretion that is rich in amylase; agonists that mobilize Ca++ elicit a secretion that is more voluminous but has a lower concentration of amylase. Ca++-mobilizing agonists may also elevate the concentration of cyclic guanosine monophosphate (cGMP), which may mediate the trophic effects evoked by these agonists.