The insulin secretory response to intravenous glucose in the rat is independent of NO formation.

In isolated pancreative beta cells from rats the insulin secretory response to glucose is amplified by L-arginine. Since this effect is inhibited by NO synthesis inhibitors, and since L-arginine is precursor of NO, the observation indicates a role for NO in insulin secretion from beta cells. We recently reported that i.v. L-arginine elicited insulin secretion in anaesthetized rats by a mechanism that was partly NO dependent. The aim of the present study was to assess if the insulin secretory response to an intravenous infusion of glucose also requires an intact NO formation. Anaesthetized rats were given D-glucose (100 mg kg-1 min-1 i.v. for 30 min). Plasma insulin (PI), blood glucose (BG) levels and mean arterial blood pressure (MAP) were assessed from before and until 15 min after the end of the infusion. One group of rats were untreated and served as controls. The two other groups were pretreated with either of the NO synthase inhibitors NW-nitro-L-arginine methyl ester (L-NAME, 50 mg kg-1 i.v.), or NG-monomethyl-L-arginine (L-NMMA, 100 mg kg-1 i.v.). In controls infusion of glucose elevated PI by up to 25 +/- 3 U L-1, and BG by up to 27 +/- 1 mmol L-1. Pretreatment with L-NAME elevated MAP from 74 +/- 6 to 132 +/- 4 mmHg, indicating that NO synthase was inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)