Effects of sodium nitroprusside on blood glucose concentration, B‐cell morphology and islet glutamate dehydrogenase activity in mice

Abstract

Mice injected with sodium nitroprusside (NaNP) exhibited a marked, transient hyperglycemia and enhanced activity of glutamate dehydrogenase in the pancreatic islets. Ultrastructurally, the islet B‐cells of NaNP‐treated mice showed expanded granular endoplasmic reticulum, prominent Golgi complex, increased amount of secretory granules, mitochondrial enlargement and vacuolation, and mitochondrion‐secretory granule complexes. Stereological analyses disclosed increased volume of endoplasmic reticulum, Golgi complex and mitochondria, and increased number of secretory granules in the B‐cells 1 h after the injection of NaNP. Isolated mouse islets exposed to NaNP showed stimulated activity of glutamate dehydrogenase both in the presence of 2 and 18 mM glucose, whereas the release of insulin was stimulated at 2 mM glucose, but inhibited at 18 mM glucose. The observations demonstrate that NaNP induces transiently altered structure and function in mouse islet B‐cells.

Whole Pancreatic Blood Flow and Islet Blood Flow in Hypovolemic Hypotension in Rats

“…This suggests that hypoten sion without hypovolemia with its associated compensatory mechanisms is not sufficient to cause the hyperinsulinemia. It should be noted in this context that nitroprusside has been reported to suppress glucose-induced in sulin release in vitro [22], but only at higher glucose concentrations than seen in the present study. Therefore the role of any phar macological actions on the insulin release in the present study is conjectural.…”

Hydralazine administration activates sympathetic preganglionic neurons whose activity mobilizes glucose and increases cardiovascular function

“…The targets of these activated SPN include the adrenal medulla (Minson et al, 1996a) but must also include the vasculature and heart in order to convey the baroreflex mediated effects. However, hypotensive stimuli also evoke increases in plasma glucose and this seems independent of the hypotensive agent used for example: hydralazine (Sanbar and de Romero, 1969;Satoh et al, 1980), sodium nitroprusside (Boquist, 1989;Staquet et al, 1965), and diazoxide (Altszuler et al, 1977). Increased plasma glucose mediated by sympathetic activation arises predominantly from stimulation of the splanchnic nerve.…”