Fluid and electrolyte transport in the small intestine.

The small intestine is in a dynamic state of secretion and absorption, the sum of which results in net absorption. Secretion is principally the result of chloride and bicarbonate extrusion through apical chloride channels after the activation of the second messengers cAMP, cGMP, and calcium. In addition to the cystic fibrosis transmembrane conductance regulator, several other candidate chloride channels have been identified and proposed to play a role in intestinal secretion, including the calcium-dependent chloride channel hCLCA1. Pathways leading to the negative control of secretion have been described that use cellular messengers, including inositol (3,4,5,6) tetrakisphosphate and phosphatidylinositol 3-kinase, which may act via basolateral potassium channels. The control of ion transport can also be viewed in terms of the enteric nervous system. The reflex neural pathways involved in enterotoxin-induced secretion have been substantiated and shown to involve 5-hydroxytryptamine, substance P, and the neurokinin 1 and 2 receptors in the sensory arm, and vasoactive intestinal peptide in the secretomotor efferents. Absorption of glucose in addition to active cotransport with sodium via the Na/glucose cotransporter protein has also been shown to occur passively through a carrier-mediated mechanism, using the membrane protein glucose transporter protein 2.