Neuronal NO synthase and its inhibitor PIN are present and influenced by glucose in the human beta-cell line CM and in rat INS-1 cells.

Nitric oxide (NO) is synthesised by different nitric oxide synthases (NOS) from L-arginine and acts as a signal transducer in a variety of cells. The neuronal isoenzyme of NOS (nNOS) was recently found in rodent beta-cells and beta-cell lines. We provide evidence that nNOS is also present in the human beta-cell line CM and that the specific inhibitor of nNOS PIN is expressed in CM and INS-1 cells.

Insulin-secreting INS-1 cells generate a novel type of poorly synchronized Ca2+ transients.

Pancreatic beta-cells have an intrinsic oscillatory Ca2+ activity supposed to be synchronized among the islets by cytoplasmic Ca2+ transients elicited by nonadrenergic, noncholinergic (NANC) neurons. To improve the understanding of this process, the cytoplasmic Ca2+ concentration ([Ca2+]i) was measured in two insulin-releasing cell lines using dual wavelength microfluorometry and the indicator fura-2. INS-1 cells but not RINm5F cells were found to generate transients of [Ca2+]i in the presence of the Ca2+ channel blocker methoxyverapamil.