GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion

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GRP nerves in pig antrum : role of GRP in vagal control of gastrin secretion. / Holst, J J; Poulsen, Steen Seier.

In: American Journal of Physiology (Consolidated), Vol. 253, No. 5 Pt 1, 11.1987, p. G643-9.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Holst, JJ & Poulsen, SS 1987, 'GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion', American Journal of Physiology (Consolidated), vol. 253, no. 5 Pt 1, pp. G643-9.

APA

Holst, J. J., & Poulsen, S. S. (1987). GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion. American Journal of Physiology (Consolidated), 253(5 Pt 1), G643-9.

Vancouver

Holst JJ, Poulsen SS. GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion. American Journal of Physiology (Consolidated). 1987 Nov;253(5 Pt 1):G643-9.

Author

Holst, J J ; Poulsen, Steen Seier. / GRP nerves in pig antrum : role of GRP in vagal control of gastrin secretion. In: American Journal of Physiology (Consolidated). 1987 ; Vol. 253, No. 5 Pt 1. pp. G643-9.

Bibtex

@article{b601f38935aa4291af2093aaf5305d58,
title = "GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion",
abstract = "We extracted gastrin-releasing peptide (GRP) and its C-terminal decapeptide corresponding to 6.4 and 6.8 pmol/g from pig antrum mucosa. By immunohistochemistry GRP was localized to mucosal, submucosal, and myenteric nerve fibers. A few nerve cell bodies were also identified. Using isolated perfused pig antrum with intact vagal innervation, we found concomitant, atropine-resistant release of GRP and gastrin during electrical stimulation of the vagal nerves. Intra-arterial GRP at 10(-11)-10(-10) mol/l caused up to fivefold, dose-dependent increases in gastrin secretion; higher doses were less effective and completely desensitized the gastrin cells for the lower doses. After desensitization, vagal stimulation no longer produced gastrin secretion. The substance P antagonist [D-Arg, D-Pro, D-Trp, Leu]-substance P, described as also antagonizing the actions of bombesin, decreased the gastrin response to GRP and abolished the effect of vagal stimulation. The available evidence strongly suggests that GRP nerves are responsible for the stimulatory vagal effects on gastrin secretion in the pig.",
keywords = "Animals, Atropine, Electric Stimulation, Gastric Mucosa, Gastrin-Releasing Peptide, Gastrins, Histocytochemistry, Immunoenzyme Techniques, Kinetics, Peptides, Pyloric Antrum, Substance P, Swine, Vagus Nerve",
author = "Holst, {J J} and Poulsen, {Steen Seier}",
year = "1987",
month = nov,
language = "English",
volume = "253",
pages = "G643--9",
journal = "American Journal of Physiology - Cell Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "5 Pt 1",

}

RIS

TY - JOUR

T1 - GRP nerves in pig antrum

T2 - role of GRP in vagal control of gastrin secretion

AU - Holst, J J

AU - Poulsen, Steen Seier

PY - 1987/11

Y1 - 1987/11

N2 - We extracted gastrin-releasing peptide (GRP) and its C-terminal decapeptide corresponding to 6.4 and 6.8 pmol/g from pig antrum mucosa. By immunohistochemistry GRP was localized to mucosal, submucosal, and myenteric nerve fibers. A few nerve cell bodies were also identified. Using isolated perfused pig antrum with intact vagal innervation, we found concomitant, atropine-resistant release of GRP and gastrin during electrical stimulation of the vagal nerves. Intra-arterial GRP at 10(-11)-10(-10) mol/l caused up to fivefold, dose-dependent increases in gastrin secretion; higher doses were less effective and completely desensitized the gastrin cells for the lower doses. After desensitization, vagal stimulation no longer produced gastrin secretion. The substance P antagonist [D-Arg, D-Pro, D-Trp, Leu]-substance P, described as also antagonizing the actions of bombesin, decreased the gastrin response to GRP and abolished the effect of vagal stimulation. The available evidence strongly suggests that GRP nerves are responsible for the stimulatory vagal effects on gastrin secretion in the pig.

AB - We extracted gastrin-releasing peptide (GRP) and its C-terminal decapeptide corresponding to 6.4 and 6.8 pmol/g from pig antrum mucosa. By immunohistochemistry GRP was localized to mucosal, submucosal, and myenteric nerve fibers. A few nerve cell bodies were also identified. Using isolated perfused pig antrum with intact vagal innervation, we found concomitant, atropine-resistant release of GRP and gastrin during electrical stimulation of the vagal nerves. Intra-arterial GRP at 10(-11)-10(-10) mol/l caused up to fivefold, dose-dependent increases in gastrin secretion; higher doses were less effective and completely desensitized the gastrin cells for the lower doses. After desensitization, vagal stimulation no longer produced gastrin secretion. The substance P antagonist [D-Arg, D-Pro, D-Trp, Leu]-substance P, described as also antagonizing the actions of bombesin, decreased the gastrin response to GRP and abolished the effect of vagal stimulation. The available evidence strongly suggests that GRP nerves are responsible for the stimulatory vagal effects on gastrin secretion in the pig.

KW - Animals

KW - Atropine

KW - Electric Stimulation

KW - Gastric Mucosa

KW - Gastrin-Releasing Peptide

KW - Gastrins

KW - Histocytochemistry

KW - Immunoenzyme Techniques

KW - Kinetics

KW - Peptides

KW - Pyloric Antrum

KW - Substance P

KW - Swine

KW - Vagus Nerve

M3 - Journal article

C2 - 2446506

VL - 253

SP - G643-9

JO - American Journal of Physiology - Cell Physiology

JF - American Journal of Physiology - Cell Physiology

SN - 0363-6143

IS - 5 Pt 1

ER -

ID: 47488551