Cholinergic, adrenergic, and PGE1 effects on cyclic nucleotides and growth in cultured corneal epithelium

Harrison D Cavanagh, A. M. Colley

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

Effecrs of adrenergic and cholinergic drugs and prostaglandin E1 on cyclic nucleotide accumulation and parameters of growth and basement membrane synthesis were examined in corneal epithelial cell cultures. 8-bromo-cGMP significantly (p<0.05) enhanced incorporation of labeled thymidine and leucine, as did acetylcholine and carbamylcholine, which elevated cGMP and decreased cAMP/cGMP ratio. Responses to acetylcholine were abolished by atropine and α-bungarotoxin. Precursor incorporation was inhibited by dibutyryl cAMP and adenosine 5'-monophosphate and by norepinephrine, epinephrine, prostaglandin E1, and theophylline, which significantly elevated cAMP levels and cAMP/cGMP ratio. Propranolol, but not phenoxybenzamine, blocked responses to effective concentrations of norepinephrine. Norepinephrine, PGE1, and dibutyryl cAMP also significantly elevated uptake of labeled glucosamine and incorporation of labeled proline into collagenase-sensitive protein or the hydroxyproline fraction of protein hydrolysates, while acetylcholine had no effect on parameters of basement membrane synthesis. Propranolol blocked responses to norepinephrine. Results were consistent with a cGMP-mediated stimulatory role of the cholinergic transmitter in corneal epithelial growth regulation, cAMP-mediated β-adrenergic suppression of regrowth and increased basement membrane production after initial injury to the corneal epithelium, and potentiation of the adrenergic effect by prostaglandins.

Original languageEnglish (US)
Pages (from-to)63-74
Number of pages12
JournalMetabolic, Pediatric and Systemic Ophthalmology
Volume6
Issue number2
StatePublished - 1982

Fingerprint

Corneal Epithelium
Alprostadil
Cyclic Nucleotides
Adrenergic Agents
Cholinergic Agents
Norepinephrine
Basement Membrane
Acetylcholine
Growth
Propranolol
Protein Hydrolysates
Bungarotoxins
Phenoxybenzamine
Glucosamine
Hydroxyproline
Carbachol
Collagenases
Adenosine Monophosphate
Theophylline
Atropine

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Ophthalmology
  • Pediatrics, Perinatology, and Child Health

Cite this

@article{b8443b3a385c4ffaa7e9522e274e1728,
title = "Cholinergic, adrenergic, and PGE1 effects on cyclic nucleotides and growth in cultured corneal epithelium",
abstract = "Effecrs of adrenergic and cholinergic drugs and prostaglandin E1 on cyclic nucleotide accumulation and parameters of growth and basement membrane synthesis were examined in corneal epithelial cell cultures. 8-bromo-cGMP significantly (p<0.05) enhanced incorporation of labeled thymidine and leucine, as did acetylcholine and carbamylcholine, which elevated cGMP and decreased cAMP/cGMP ratio. Responses to acetylcholine were abolished by atropine and α-bungarotoxin. Precursor incorporation was inhibited by dibutyryl cAMP and adenosine 5'-monophosphate and by norepinephrine, epinephrine, prostaglandin E1, and theophylline, which significantly elevated cAMP levels and cAMP/cGMP ratio. Propranolol, but not phenoxybenzamine, blocked responses to effective concentrations of norepinephrine. Norepinephrine, PGE1, and dibutyryl cAMP also significantly elevated uptake of labeled glucosamine and incorporation of labeled proline into collagenase-sensitive protein or the hydroxyproline fraction of protein hydrolysates, while acetylcholine had no effect on parameters of basement membrane synthesis. Propranolol blocked responses to norepinephrine. Results were consistent with a cGMP-mediated stimulatory role of the cholinergic transmitter in corneal epithelial growth regulation, cAMP-mediated β-adrenergic suppression of regrowth and increased basement membrane production after initial injury to the corneal epithelium, and potentiation of the adrenergic effect by prostaglandins.",
author = "Cavanagh, {Harrison D} and Colley, {A. M.}",
year = "1982",
language = "English (US)",
volume = "6",
pages = "63--74",
journal = "Metabolic, pediatric, and systemic ophthalmology",
issn = "0277-9382",
publisher = "Opto Education Corporation",
number = "2",

}

TY - JOUR

T1 - Cholinergic, adrenergic, and PGE1 effects on cyclic nucleotides and growth in cultured corneal epithelium

AU - Cavanagh, Harrison D

AU - Colley, A. M.

PY - 1982

Y1 - 1982

N2 - Effecrs of adrenergic and cholinergic drugs and prostaglandin E1 on cyclic nucleotide accumulation and parameters of growth and basement membrane synthesis were examined in corneal epithelial cell cultures. 8-bromo-cGMP significantly (p<0.05) enhanced incorporation of labeled thymidine and leucine, as did acetylcholine and carbamylcholine, which elevated cGMP and decreased cAMP/cGMP ratio. Responses to acetylcholine were abolished by atropine and α-bungarotoxin. Precursor incorporation was inhibited by dibutyryl cAMP and adenosine 5'-monophosphate and by norepinephrine, epinephrine, prostaglandin E1, and theophylline, which significantly elevated cAMP levels and cAMP/cGMP ratio. Propranolol, but not phenoxybenzamine, blocked responses to effective concentrations of norepinephrine. Norepinephrine, PGE1, and dibutyryl cAMP also significantly elevated uptake of labeled glucosamine and incorporation of labeled proline into collagenase-sensitive protein or the hydroxyproline fraction of protein hydrolysates, while acetylcholine had no effect on parameters of basement membrane synthesis. Propranolol blocked responses to norepinephrine. Results were consistent with a cGMP-mediated stimulatory role of the cholinergic transmitter in corneal epithelial growth regulation, cAMP-mediated β-adrenergic suppression of regrowth and increased basement membrane production after initial injury to the corneal epithelium, and potentiation of the adrenergic effect by prostaglandins.

AB - Effecrs of adrenergic and cholinergic drugs and prostaglandin E1 on cyclic nucleotide accumulation and parameters of growth and basement membrane synthesis were examined in corneal epithelial cell cultures. 8-bromo-cGMP significantly (p<0.05) enhanced incorporation of labeled thymidine and leucine, as did acetylcholine and carbamylcholine, which elevated cGMP and decreased cAMP/cGMP ratio. Responses to acetylcholine were abolished by atropine and α-bungarotoxin. Precursor incorporation was inhibited by dibutyryl cAMP and adenosine 5'-monophosphate and by norepinephrine, epinephrine, prostaglandin E1, and theophylline, which significantly elevated cAMP levels and cAMP/cGMP ratio. Propranolol, but not phenoxybenzamine, blocked responses to effective concentrations of norepinephrine. Norepinephrine, PGE1, and dibutyryl cAMP also significantly elevated uptake of labeled glucosamine and incorporation of labeled proline into collagenase-sensitive protein or the hydroxyproline fraction of protein hydrolysates, while acetylcholine had no effect on parameters of basement membrane synthesis. Propranolol blocked responses to norepinephrine. Results were consistent with a cGMP-mediated stimulatory role of the cholinergic transmitter in corneal epithelial growth regulation, cAMP-mediated β-adrenergic suppression of regrowth and increased basement membrane production after initial injury to the corneal epithelium, and potentiation of the adrenergic effect by prostaglandins.

UR - http://www.scopus.com/inward/record.url?scp=0020333803&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020333803&partnerID=8YFLogxK

M3 - Article

C2 - 6298565

AN - SCOPUS:0020333803

VL - 6

SP - 63

EP - 74

JO - Metabolic, pediatric, and systemic ophthalmology

JF - Metabolic, pediatric, and systemic ophthalmology

SN - 0277-9382

IS - 2

ER -