Cholinergic-adrenergic interactions on intestinal ion transport

E. J. Tapper, D. W. Powell, S. M. Morris

Research output: Contribution to journalArticle

Abstract

The autonomic control of intestinal electrolyte transport has been investigated in the in vitro, short-circuited rabbit ileum with varying doses of carbachol and with neuroeffector blocking agents. Low-dose carbachol (<10-6 M) and high-dose carbachol (>10-4 M) had different effects on Na and Cl transport. Low-dose carbachol caused a transient increase in the potential difference and short-circuit current, stimulated Cl secretion, and inhibited the residual flux (probably HCO3 secretion). This is a muscarinic response since it is inhibited by atropine (10-6 M). After an initial increase of the potential difference and short-circuit current, high-dose carbachol reduced these electrical parameters, stimulated Na and Cl absorption, and abolished the residual flux. This is a nicotinic response since it is inhibited by hexamethonium (10-5 M). This nicotinic response is identical to that reported by others with α-adrenergic agents and it was inhibited also by phentolamine (10-7 M). The authors propose high-dose carbachol stimulates nicotinic receptors on postganglionic sympathetic fibers present in their preparations causing a release of catecholamines and a resulting α-adrenergic response by the intestinal epithelial cell. The physiological significance of this response in the gut remains to be determined.

Original languageEnglish (US)
JournalAmerican Journal of Physiology Endocrinology Metabolism and Gastrointestinal Physiology
Volume4
Issue number4
StatePublished - 1978
Externally publishedYes

Fingerprint

Ion Transport
Carbachol
Adrenergic Agents
Cholinergic Agents
Postganglionic Sympathetic Fibers
Hexamethonium
Phentolamine
Nicotinic Receptors
Atropine
Ileum
Electrolytes
Catecholamines
Epithelial Cells
Rabbits

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Cholinergic-adrenergic interactions on intestinal ion transport. / Tapper, E. J.; Powell, D. W.; Morris, S. M.

In: American Journal of Physiology Endocrinology Metabolism and Gastrointestinal Physiology, Vol. 4, No. 4, 1978.

Research output: Contribution to journalArticle

@article{5c880fd8af8d409f8b88291bd226d65f,
title = "Cholinergic-adrenergic interactions on intestinal ion transport",
abstract = "The autonomic control of intestinal electrolyte transport has been investigated in the in vitro, short-circuited rabbit ileum with varying doses of carbachol and with neuroeffector blocking agents. Low-dose carbachol (<10-6 M) and high-dose carbachol (>10-4 M) had different effects on Na and Cl transport. Low-dose carbachol caused a transient increase in the potential difference and short-circuit current, stimulated Cl secretion, and inhibited the residual flux (probably HCO3 secretion). This is a muscarinic response since it is inhibited by atropine (10-6 M). After an initial increase of the potential difference and short-circuit current, high-dose carbachol reduced these electrical parameters, stimulated Na and Cl absorption, and abolished the residual flux. This is a nicotinic response since it is inhibited by hexamethonium (10-5 M). This nicotinic response is identical to that reported by others with α-adrenergic agents and it was inhibited also by phentolamine (10-7 M). The authors propose high-dose carbachol stimulates nicotinic receptors on postganglionic sympathetic fibers present in their preparations causing a release of catecholamines and a resulting α-adrenergic response by the intestinal epithelial cell. The physiological significance of this response in the gut remains to be determined.",
author = "Tapper, {E. J.} and Powell, {D. W.} and Morris, {S. M.}",
year = "1978",
language = "English (US)",
volume = "4",
journal = "American Journal of Physiology Endocrinology Metabolism and Gastrointestinal Physiology",
issn = "0363-6100",
publisher = "American Physiological Society",
number = "4",

}

TY - JOUR

T1 - Cholinergic-adrenergic interactions on intestinal ion transport

AU - Tapper, E. J.

AU - Powell, D. W.

AU - Morris, S. M.

PY - 1978

Y1 - 1978

N2 - The autonomic control of intestinal electrolyte transport has been investigated in the in vitro, short-circuited rabbit ileum with varying doses of carbachol and with neuroeffector blocking agents. Low-dose carbachol (<10-6 M) and high-dose carbachol (>10-4 M) had different effects on Na and Cl transport. Low-dose carbachol caused a transient increase in the potential difference and short-circuit current, stimulated Cl secretion, and inhibited the residual flux (probably HCO3 secretion). This is a muscarinic response since it is inhibited by atropine (10-6 M). After an initial increase of the potential difference and short-circuit current, high-dose carbachol reduced these electrical parameters, stimulated Na and Cl absorption, and abolished the residual flux. This is a nicotinic response since it is inhibited by hexamethonium (10-5 M). This nicotinic response is identical to that reported by others with α-adrenergic agents and it was inhibited also by phentolamine (10-7 M). The authors propose high-dose carbachol stimulates nicotinic receptors on postganglionic sympathetic fibers present in their preparations causing a release of catecholamines and a resulting α-adrenergic response by the intestinal epithelial cell. The physiological significance of this response in the gut remains to be determined.

AB - The autonomic control of intestinal electrolyte transport has been investigated in the in vitro, short-circuited rabbit ileum with varying doses of carbachol and with neuroeffector blocking agents. Low-dose carbachol (<10-6 M) and high-dose carbachol (>10-4 M) had different effects on Na and Cl transport. Low-dose carbachol caused a transient increase in the potential difference and short-circuit current, stimulated Cl secretion, and inhibited the residual flux (probably HCO3 secretion). This is a muscarinic response since it is inhibited by atropine (10-6 M). After an initial increase of the potential difference and short-circuit current, high-dose carbachol reduced these electrical parameters, stimulated Na and Cl absorption, and abolished the residual flux. This is a nicotinic response since it is inhibited by hexamethonium (10-5 M). This nicotinic response is identical to that reported by others with α-adrenergic agents and it was inhibited also by phentolamine (10-7 M). The authors propose high-dose carbachol stimulates nicotinic receptors on postganglionic sympathetic fibers present in their preparations causing a release of catecholamines and a resulting α-adrenergic response by the intestinal epithelial cell. The physiological significance of this response in the gut remains to be determined.

UR - http://www.scopus.com/inward/record.url?scp=0018255390&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0018255390&partnerID=8YFLogxK

M3 - Article

VL - 4

JO - American Journal of Physiology Endocrinology Metabolism and Gastrointestinal Physiology

JF - American Journal of Physiology Endocrinology Metabolism and Gastrointestinal Physiology

SN - 0363-6100

IS - 4

ER -