Studies on diazoxide hyperglycemia in rats have shown the blood glucose response to orally administered diazoxide to be dose-related with a peak effect at five hours following dosage. Diazoxide hyperglycemia could be reversed by the administration of tolbutamide. Plasma insulin-like activity was not decreased by diazoxide nor was the insulin-mediated increase in L-arabinose distribution affected. Both hypophysectomy and adrenalectomy reduced the hyperglycemic response to diazoxide. In addition, plasma corticosteroid levels were found to be significantly elevated five hours following the drug. The hyperglycemic response to diazoxide could be reduced by prior treatment with the beta-adrenergic blocking drug, MJ 1999 [4-(2-isopropylamino-l-hydroxyethyl) methane-sulfonanilide HCl]. Further studies showed that potassium deficiency resulted in an exaggerated hyperglycemic response to diazoxide; this response, as well as that produced in normal animals, could be antagonized by administration of potassium chloride. In addition, glucose tolerance was somewhat decreased by subhyperglycemic doses of diazoxide, especially in potassium deficient animals. It is suggested that adrenergic influences are a significant component of diazoxide hyperglycemia. The potassium changes are thought merely to alter the sensitivity of the sympathetic elements or receptors.

This content is only available via PDF.