Segment-specific effects of epinephrine on ion transport in the colon of the rat

Abstract

The effect of epinephrine on transport of K+, Na+, Cl−, and[Formula: see text] across the rat colon was studied using the Ussing chamber technique. Epinephrine (5 × 10−6 mol/l) induced a biphasic change in short-circuit current ( I sc) in distal and proximal colon: a transient increase followed by a long-lasting decay. The first phase of the I sc response was abolished in Cl−-poor solution or after bumetanide administration, indicating a transient induction of Cl− secretion. The second phase of the response to epinephrine was suppressed by apical administration of the K+channel blocker, quinine, and was concomitant with an increase in serosal-to-mucosal Rb+ flux, indicating that epinephrine induced K+ secretion, although this response was much smaller than the change in I sc. In addition, the distal colon displayed a decrease in mucosal-to-serosal and serosal-to-mucosal Cl−fluxes when treated with epinephrine. In the distal colon, indomethacin abolished the first phase of the epinephrine effect, whereas the second phase was suppressed by TTX. In the proximal colon, indomethacin and TTX were ineffective. The neuronally mediated response to epinephrine in the distal colon was suppressed by the nonselective β-receptor blocker, propranolol, and by the β2-selective blocker, ICI-118551, whereas the epithelial response in the proximal colon was suppressed by the nonselective α-blocker, phentolamine, and by the selective α2-blocker, yohimbine. These results indicate a segment-specific action of epinephrine on ion transport: a direct stimulatory action on epithelial α2-receptors in the proximal colon and an indirect action on secretomotoneurons via β2-receptors in the distal colon.

Global Effects of the Cell-to-Cell Signaling Molecules Autoinducer-2, Autoinducer-3, and Epinephrine in a luxS Mutant of Enterohemorrhagic Escherichia coli

“…The stress hormones epinephrine and norepinephrine are present in the gastrointestinal tract and modulate smooth muscle contraction, submucosal blood flow, and chloride and potassium secretion there (29). Norepinephrine is produced within adrenergic neurons present in the enteric nervous system (20), whereas epinephrine is synthesized in both the central nervous system and the adrenal medulla and is involved in systemic responses (48).…”

The two-component system QseEF and the membrane protein QseG link adrenergic and stress sensing to bacterial pathogenesis

“…Norepinephrine is produced in the intestine by adrenergic neurons of the enteric nervous system, whereas Epi is a systemic hormone produced in the central nervous system and the adrenal medulla that reaches the intestine through the bloodstream (13,14). These stress hormones affect many normal functions of the intestine, such as chloride and potassium secretion (13)(14)(15). Upon recognition of these signals, QseC autophosphorylates, then transfers a phosphate to QseB, which in turn activates the flagella regulon (2) and genes involved in AE lesion (3).…”

A Novel Two-Component Signaling System That Activates Transcription of an Enterohemorrhagic Escherichia coli Effector Involved in Remodeling of Host Actin

“…Although epinephrine is not synthesized in the enteric nervous system, it is synthesized in the central nervous system and in the adrenal medulla, where it is released into the bloodstream and acts in a systemic manner, eventually reaching the intestine (31). Both hormones modulate intestinal smooth muscle contraction, submucosal blood flow, and chloride and potassium secretion in the intestine, all important during bacterial infection (17). The EHEC sensor kinase, QseC, autophosphorylates in response to each of these signals (6) and initiates a complex signaling cascade that regulates the expression of genes encoding proteins necessary for AE lesion formation and the flagellar regulon (6)(7)(8)(34)(35)(36).…”