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Albert Salehi

S Albert Salehi

Research team manager

Albert Salehi

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

Author

  • S Albert Salehi
  • Fariborz Parandeh
  • Ingmar Lundquist

Summary, in English

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.

Department/s

  • Islet cell physiology

Publishing year

1998

Language

English

Pages

19-28

Publication/Series

Bioscience Reports

Volume

18

Issue

1

Document type

Journal article

Publisher

Kluwer

Topic

  • Endocrinology and Diabetes

Keywords

  • Insulin and glucagon secretion
  • isolated mouse islets
  • nitric oxide synthase
  • NG-nitro-L-arginine methyl ester
  • L-arginine
  • diazoxide
  • glucose
  • high K+

Status

Published

Research group

  • Islet cell physiology

ISBN/ISSN/Other

  • ISSN: 0144-8463