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The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester potentiates insulin secretion stimulated by glucose and L-arginine independently of its action on ATP-sensitive K+ channels

Salehi, S Albert LU orcid ; Parandeh, Fariborz and Lundquist, Ingmar LU (1998) In Bioscience Reports 18(1). p.19-28
Abstract
The nature of the action of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on hormone release from isolated islets was investigated. We found that glucose-induced insulin release was potentiated by L-NAME in the absence or presence of diazoxide, a potent K+ATP channel opener, as well as in the presence of diazoxide plus a depolarizing concentration of K+. At a low, physiological glucose concentration L-NAME did not influence insulin secretion induced by K+ but inhibited glucagon secretion. L-arginine-induced insulin release was potentiated by L-NAME. This potentiation was observed also in the presence of K+ plus diazoxide. Further, glucagon release induced by L-arginine as well as by L-arginine plus K+... (More)
The nature of the action of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on hormone release from isolated islets was investigated. We found that glucose-induced insulin release was potentiated by L-NAME in the absence or presence of diazoxide, a potent K+ATP channel opener, as well as in the presence of diazoxide plus a depolarizing concentration of K+. At a low, physiological glucose concentration L-NAME did not influence insulin secretion induced by K+ but inhibited glucagon secretion. L-arginine-induced insulin release was potentiated by L-NAME. This potentiation was observed also in the presence of K+ plus diazoxide. Further, glucagon release induced by L-arginine as well as by L-arginine plus K+ and diazoxide was suppressed by L-NAME. The results strongly suggest that the L-NAME-induced potentiation of insulin secretion in response to glucose or L-arginine as well as the inhibitory effects on glucagon secretion are largely mediated by L-NAME directly suppressing islet NOS activity. Hence NO apparently affects insulin and glucagon secretion independently of membrane depolarization events. (Less)
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author
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publishing date
type
Contribution to journal
publication status
published
subject
keywords
Insulin and glucagon secretion, isolated mouse islets, nitric oxide synthase, NG-nitro-L-arginine methyl ester, L-arginine, diazoxide, glucose, high K+
in
Bioscience Reports
volume
18
issue
1
pages
19 - 28
publisher
Portland Press
external identifiers
  • pmid:9653515
  • scopus:0031817046
ISSN
0144-8463
DOI
10.1023/A:1022288600348
language
English
LU publication?
yes
id
4ff9cfc3-0f84-4f42-8fff-9983b27ecf51 (old id 1113492)
date added to LUP
2016-04-01 15:18:01
date last changed
2025-04-04 14:48:34
@article{4ff9cfc3-0f84-4f42-8fff-9983b27ecf51,
  abstract     = {{The nature of the action of the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on hormone release from isolated islets was investigated. We found that glucose-induced insulin release was potentiated by L-NAME in the absence or presence of diazoxide, a potent K+ATP channel opener, as well as in the presence of diazoxide plus a depolarizing concentration of K+. At a low, physiological glucose concentration L-NAME did not influence insulin secretion induced by K+ but inhibited glucagon secretion. L-arginine-induced insulin release was potentiated by L-NAME. This potentiation was observed also in the presence of K+ plus diazoxide. Further, glucagon release induced by L-arginine as well as by L-arginine plus K+ and diazoxide was suppressed by L-NAME. The results strongly suggest that the L-NAME-induced potentiation of insulin secretion in response to glucose or L-arginine as well as the inhibitory effects on glucagon secretion are largely mediated by L-NAME directly suppressing islet NOS activity. Hence NO apparently affects insulin and glucagon secretion independently of membrane depolarization events.}},
  author       = {{Salehi, S Albert and Parandeh, Fariborz and Lundquist, Ingmar}},
  issn         = {{0144-8463}},
  keywords     = {{Insulin and glucagon secretion; isolated mouse islets; nitric oxide synthase; NG-nitro-L-arginine methyl ester; L-arginine; diazoxide; glucose; high K+}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{19--28}},
  publisher    = {{Portland Press}},
  series       = {{Bioscience Reports}},
  title        = {{The nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester potentiates insulin secretion stimulated by glucose and L-arginine independently of its action on ATP-sensitive K+ channels}},
  url          = {{http://dx.doi.org/10.1023/A:1022288600348}},
  doi          = {{10.1023/A:1022288600348}},
  volume       = {{18}},
  year         = {{1998}},
}