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Am J Physiol Endocrinol Metab 279: E95-E107, 2000;
0193-1849/00 $5.00
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Vol. 279, Issue 1, E95-E107, July 2000

Chronic blockade of NO synthase paradoxically increases islet NO production and modulates islet hormone release

Ragnar Henningsson1, Per Alm2, Erik Lindström1, and Ingmar Lundquist1

Institute of Physiological Sciences, 1 Departments of Pharmacology and 2 Pathology, University of Lund, Lund, Sweden

Islet production of nitric oxide (NO) and CO in relation to islet hormone secretion was investigated in mice given the NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) in their drinking water. In these mice, the total islet NO production was paradoxically increased, reflecting induction of inducible NOS (iNOS) in background of reduced activity and immunoreactivity of constitutive NOS (cNOS). Unexpectedly, normal mice fasted for 24 h also displayed iNOS activity, which was further increased in L-NAME-drinking mice. Glucose-stimulated insulin secretion in vitro and in vivo was increased in fasted but unaffected in fed mice after L-NAME drinking. Glucagon secretion was increased in vitro. Control islets incubated with different NOS inhibitors at 20 mM glucose displayed increased insulin release and decreased cNOS activity. These NOS inhibitors potentiated glucose-stimulated insulin release also from islets of L-NAME-drinking mice. In contrast, glucagon release was suppressed. In islets from L-NAME-drinking mice, cyclic nucleotides were upregulated, and forskolin-stimulated hormone release, CO production, and heme oxygenase (HO)-2 expression increased. In conclusion, chronic NOS blockade evoked iNOS-derived NO production in pancreatic islets and elicited compensatory mechanisms against the inhibitory action of NO on glucose-stimulated insulin release by inducing upregulation of the islet cAMP and HO-CO systems.

chronic nitric oxide synthase blockade; nitric oxide and carbon monoxide; insulin and glucagon secretion; isolated islets; cyclic nucleotides


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