Taste receptors in the gastrointestinal tract. V. Acid sensing in the gastrointestinal tract

Abstract

Luminal acidity is a physiological challenge in the foregut, and acidosis can occur throughout the gastrointestinal tract as a result of inflammation or ischemia. These conditions are surveyed by an elaborate network of acid-governed mechanisms to maintain homeostasis. Deviations from physiological values of extracellular pH are monitored by multiple acid sensors expressed by epithelial cells and sensory neurons. Acid-sensing ion channels are activated by moderate acidification, whereas transient receptor potential ion channels of the vanilloid subtype are gated by severe acidosis. Some ionotropic purinoceptor ion channels and two-pore domain background K(+) channels are also sensitive to alterations of extracellular pH.

Figure 1

Two types of luminal acid-induced programs to ensure tissue homeostasis in the esophagus, stomach and duodenum. Either type of program is under the control of molecular acid sensors (AS) on sensory neurons. CNS, central nervous system; ENS, enteric nervous system; LES, lower esophageal sphincter.

Figure 2

Membrane topology of four classes of acid-sensitive ion channel subunits relevant to acid sensing in the GI tract: ASIC (acid-sensing ion channel), TRPV (transient receptor potential ion channel of the vanilloid subtype), P2X (ionotropic purinoceptor), and KCNK (two pore domain potassium channel). A, ankyrin; C, C-terminal; N, N-terminal; P, pore; TM, transmembrane domain.