Imidazoline‐induced amplification of glucose‐ and carbachol‐stimulated insulin release includes a marked suppression of islet nitric oxide generation in the mouse

Abstract

RX effectively counteracts the negative impact of beta-cell NO generation on insulin release stimulated by glucose and carbachol suggesting imidazoline compounds by virtue of NOS inhibitory properties being of potential therapeutic value for treatment of beta-cell dysfunction in hyperglycaemia and type 2 diabetes.