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Neurohormonal Control of Fluid and Electrolyte Transport in Intestinal Mucosa

David R. Brown, Richard J. Miller

10.1002/cphy.cp060424

Source: Supplement 19: Handbook of Physiology, The Gastrointestinal System, Intestinal Absorption and Secretion

Originally published: 1991

Published online: January 2011

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Regulation By Amine Neurotransmitter Substances
1.1 Acetylcholine
1.2 Norepinephrine and Other Catecholamines
1.3 5‐Hydroxytryptamine
1.4 Histamine
2 Regulation by Purines
3 Regulation by Circulating Hormones Involved in Fluid and Ion Homeostasis
3.1 Angiotensin
3.2 Vasopressin
3.3 Atrial Natriuretic Peptides
4 Regulation by Neurogastrointestinal Peptides
4.1 Background
4.2 Substances Having Proabsorptive or Antisecretory Action
4.3 Substances Having Secretory or Antiabsorptive Action
5 Intrinsic Neural Control of Mucosal Ion Transport
6 Regulation by Central Nervous System
7 Summary and Future Directions
Figure 1. Figure 1.

Arrangement of enteric plexuses.

[From Furness and Costa 252. In Cell and Tissue Research, © 1978, Raven Press, New York.]
Figure 2. Figure 2.

Proposed model of neural control of ion transport by guinea pig small intestinal mucosa. Physical or intraluminal chemical stimuli activate sensory neurons within the gut wall to release acetylcholine (Ach). Acetylcholine acts at nicotinic receptors on neurons in submucosal or mucosal plexuses or on epithelial cell muscarinic receptors. Acetylcholinergic neuronal activity in these plexuses is enhanced or suppressed by input from myenteric neurons containing serotonin (5‐HT) or enkephalin (ENK), respectively. Extrinsic norepinephrine (NE)/somatostatin (SOM)–containing neurons originating in prevertebral ganglia inhibit spontaneous activity in submucous plexus and also act directly on transporting cells to promote electrolyte absorption. M. mucosae, muscularis mucosae; circ. muscle, circular muscle; long, muscle, longitudinal muscle.

[From Cooke 128. Copyright 1986 by The American Gastroenterological Association.]
Figure 3. Figure 3.

Effect of electrical field stimulation (horizontal line) on mucosal (M)‐to‐serosal (S) (open circles) and serosal‐to‐mucosal (filled circles) fluxes of 36Cl− across the guinea pig ileal mucosa mounted in an Ussing chamber apparatus.

[From Cooke et al. 133.]
Figure 4. Figure 4.

Proposed model of mechanism by which opioid peptides, administered into cerebral ventricles, might produce proabsorptive or antisecretory actions in upper small intestine of rat. Intracerebroventricular administration of opioid peptides, particularly those acting on central nervous system δ or μ‐opiate receptors may activate sympathetic nerves (via celiac ganglion) projecting to proximal jejunum. Release of norepinephrine from sympathetic nerve terminals inhibits actions of transmitters that promote active Cl− secretion. Norepinephrine may additionally act at α2‐adrenergic receptors on transporting enterocytes to promote NaCl absorption. +, Stimulatory influence; ‐, inhibitory influence.
Figure 5. Figure 5.

Probable model of neuronal reflex arc in the gut wall affecting intestinal ion transport. Sensory receptors located in muscle layers or mucosa detect changes in gut mechanical activity or luminal composition that transmit this information through interneurons in enteric ganglionated plexuses. This results in activation of specific motor or effector neurons that synapse on basolateral membranes of transporting enterocytes and elicit changes in ion transport by these cells.

[From Cooke 688. In Physiology of the Gastrointestinal Tract, © 1987, Raven Press, New York.]


Figure 1.

Arrangement of enteric plexuses.

[From Furness and Costa 252. In Cell and Tissue Research, © 1978, Raven Press, New York.]


Figure 2.

Proposed model of neural control of ion transport by guinea pig small intestinal mucosa. Physical or intraluminal chemical stimuli activate sensory neurons within the gut wall to release acetylcholine (Ach). Acetylcholine acts at nicotinic receptors on neurons in submucosal or mucosal plexuses or on epithelial cell muscarinic receptors. Acetylcholinergic neuronal activity in these plexuses is enhanced or suppressed by input from myenteric neurons containing serotonin (5‐HT) or enkephalin (ENK), respectively. Extrinsic norepinephrine (NE)/somatostatin (SOM)–containing neurons originating in prevertebral ganglia inhibit spontaneous activity in submucous plexus and also act directly on transporting cells to promote electrolyte absorption. M. mucosae, muscularis mucosae; circ. muscle, circular muscle; long, muscle, longitudinal muscle.

[From Cooke 128. Copyright 1986 by The American Gastroenterological Association.]


Figure 3.

Effect of electrical field stimulation (horizontal line) on mucosal (M)‐to‐serosal (S) (open circles) and serosal‐to‐mucosal (filled circles) fluxes of 36Cl− across the guinea pig ileal mucosa mounted in an Ussing chamber apparatus.

[From Cooke et al. 133.]


Figure 4.

Proposed model of mechanism by which opioid peptides, administered into cerebral ventricles, might produce proabsorptive or antisecretory actions in upper small intestine of rat. Intracerebroventricular administration of opioid peptides, particularly those acting on central nervous system δ or μ‐opiate receptors may activate sympathetic nerves (via celiac ganglion) projecting to proximal jejunum. Release of norepinephrine from sympathetic nerve terminals inhibits actions of transmitters that promote active Cl− secretion. Norepinephrine may additionally act at α2‐adrenergic receptors on transporting enterocytes to promote NaCl absorption. +, Stimulatory influence; ‐, inhibitory influence.



Figure 5.

Probable model of neuronal reflex arc in the gut wall affecting intestinal ion transport. Sensory receptors located in muscle layers or mucosa detect changes in gut mechanical activity or luminal composition that transmit this information through interneurons in enteric ganglionated plexuses. This results in activation of specific motor or effector neurons that synapse on basolateral membranes of transporting enterocytes and elicit changes in ion transport by these cells.

[From Cooke 688. In Physiology of the Gastrointestinal Tract, © 1987, Raven Press, New York.]
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Article Title: Neurohormonal Control of Fluid and Electrolyte Transport in Intestinal Mucosa
 

How to Cite

David R. Brown, Richard J. Miller. Neurohormonal Control of Fluid and Electrolyte Transport in Intestinal Mucosa. Compr Physiol 2011, Supplement 19: Handbook of Physiology, The Gastrointestinal System, Intestinal Absorption and Secretion: 527-589. First published in print 1991. doi: 10.1002/cphy.cp060424