Abstract
The direct effects of the hyperglycemic agent diazoxide (D), on dynamic insulin (IRI) release from rat pancreas in vitro have been compared with those of epinephrine (E). Like E, D produces dose dependent suppression of the primary (I) and secondary (II) phases of glucose (G) induced IRI release, an effect partly reversed by α adrenergic blockade. Conversely, continuous stimulation with 10 μg/ml + 20 μg/ml phentolamine produces a biphasic pattern of IRI release similar to that observed with β adrenergic stimulation with I-isopropylnorepinephrine, either agent alone being ineffective. As for E, prestimuation with low doses of D selectively enhances subsequent G induced I, an effect abolished by β adrenergic blockade during prestim. In contrast to E, prestim. with higher concentrations of D enhances both phases of G induced IRI release, an effect whifh is not abolished by α adren. blockade during prestim. conclusions: (a) D can stimulate both α adrenergic receptor activity in B cells which may explain both the direct inhibition of IRI release by D and the apparently paradoxical enhancement of IRI release on cessation of D therapy. (b) Some effects of D are not realized through direct effects on adrenergic receptors.
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Burr, I., Marliss, E., Renold, A. et al. Direct “adrenergic” activity of diazoxide on insulin release. Pediatr Res 5, 397 (1971). https://doi.org/10.1203/00006450-197108000-00108
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DOI: https://doi.org/10.1203/00006450-197108000-00108