The foregoing description of digestion has stressed that these processes take place in the small intestine in an aqueous •Fig. 30.16 OverallfluidbalanceinthehumanGItract.About1to2Lofwaterisingested,and8LofvarioussecretionsenterstheGItract.Ofthistotal,mostisabsorbedinthesmallintestine.About2Lispassedontothecolon,thevastmajorityofwhichisabsorbedinhealth.(FromVanderAJetal.Human Physiology. 6thed.NewYork:McGraw-Hill;1994.) milieu. The fluidity of intestinal contents, especially in the small intestine, is important in allowing the meal to be propelled along the length of the intestine and to permit digested nutrients to diffuse to their site of absorption. Part of this fluid is derived from oral intake, but in most adults this consists of only about 1 to 2 L/day derived from both food and drink (Fig. 30.16 ). Additional fluid is supplied by the stomach and the small intestine themselves, as well as the organs that drain into the GI tract. In total, these secretions add another 8 L, which means that the intestine is presented with approximately 9 to 10 L of fluid on a daily basis. However, in health only about 2 L of this load is passed to the colon for reabsorption, and eventually only 100 to 200 mL exits in stool. Thus the intestine absorbs water overall. During the postprandial period, such absorption is promoted in the small intestine predominantly via the osmotic effects of nutrient absorption. An osmotic gradient is established across the intestinal epithelium that simultaneously drives movement of water across the tight junctions. The generic mechanism for nutrient-driven Na+ and water absorption in the small intestine is diagrammed in
Fig. 30.17 . Moreover, in the period between meals, when nutrients are absent, fluid absorption can still occur via the coupled uptake of Na+ and Cl− mediated by the cooperative interaction of a Na+/H+ antiporter (NHE-3) and a Cl−/ HCO3 − antiporter (see
Fig. 30.17
Even though net water and electrolyte transport in the small intestine is predominantly absorptive, this does not imply that the tissue fails to participate in electrolyte secretion. Secretion is regulated in response to signals derived from the luminal contents and in response to deformation of the mucosa and intestinal distention. Critical secretagogues include acetylcholine, VIP, prostaglandins, and serotonin. Secretion ensures that the intestinal contents are appropriately fluid while digestion and absorption are ongoing and is important to lubricate the passage of food particles along the length of the intestine. For example, some clinical evidence suggests that constipation and intestinal obstruction, the latter observed in cystic fibrosis, can result when secretion is abnormally low. The majority of the intestinal •Fig. 30.17 MechanismsofNaClabsorptioninthesmallintestine.DRA,downregulatedinadenoma;GLUT2,glucosetransporter2;KCC1,potassium/chloridecotransporter1;NHE-3,sodium/hydrogenexchanger3;PAT1,putativeaniontransporter1;SGLT1,sodium/glucosetransporter1.SGLT1H˜2K˜KCC1NHE 3DRA?PAT1?ATPHCO3°GLUT2Glucose secretory flow of fluid into the lumen is driven by active secretion of chloride ions via the mechanism diagrammed in
Fig. 30.18 . In cystic fibrosis the loss of CFTR Cl channels can partially be compensated for by accessory chloride channels, such as the TMEM16A channel that is activated by elevations in cytoplasmic calcium. Some segments of the intestine may engage in additional secretory mechanisms, such as secretion of bicarbonate ions via the mechanisms shown in