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

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.

• Author: S Albert Salehi; Fariborz Parandeh; Ingmar Lundquist
• Department/s: Islet cell physiology
• Publishing year: 1998
• Language: English
• Pages: 19-28
• Publication/Series: Bioscience Reports
• Volume: 18
• Issue: 1
• Links: http://dx.doi.org/10.1023/A:1022288600348
• Document type: Journal article
• Publisher: Portland Press
• 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