Compounds > 2-(2-imidazolin-2-yl)-1-phenyl-1h-indole

2-(2-imidazolin-2-yl)-1-phenyl-1h-indole and Pancreatic-Neoplasms

2-(2-imidazolin-2-yl)-1-phenyl-1h-indole has been researched along with Pancreatic-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for 2-(2-imidazolin-2-yl)-1-phenyl-1h-indole and Pancreatic-Neoplasms

Article	Year
Different modes of action of the imidazoline compound RX871024 in pancreatic beta-cells. Blocking of K+ channels, mobilization of Ca2+ from endoplasmic reticulum, and interaction with exocytotic machinery. Annals of the New York Academy of Sciences, 1999, Jun-21, Volume: 881 The imidazoline compound RX871024 glucose-dependently potentiates the release of insulin in pancreatic islets and beta-cell lines. This activity of the compound is not related to its action by stimulating alpha 2-adrenoceptors and I1- and I2-imidazoline receptors. There are at least three modes of action of RX871024 in beta-cells: (1) RX871024 blocks the ATP-dependent, Ca(2+)-activated, and delayed rectifier K+ channel activity; (2) RX871024 causes mobilization of Ca2+ from thapsigargin-sensitive intracellular stores, the effect probably controlled by cytochrome P450; and (3) the stimulatory activity of RX871024 on insulin release involves interaction of the compound with the exocytotic machinery, unrelated to the changes in membrane potential and cytoplasmic-free Ca2+ concentration, whereas protein phosphorylation plays an important role in this process. The maximal insulinotropic effect of RX871024 is much higher than that of the sulfonylurea glibenclamide. RX871024 stimulates insulin release and normalizes blood glucose levels in rats in vivo without affecting blood pressure and heart rate. Topics: Animals; Blood Glucose; Blood Pressure; Calcium; Cells, Cultured; Cytoplasm; Endoplasmic Reticulum; Exocytosis; Heart Rate; Imidazoles; Indoles; Insulin; Insulin Secretion; Insulinoma; Islets of Langerhans; Kinetics; Male; Membrane Potentials; Models, Biological; Pancreatic Neoplasms; Phosphorylation; Potassium Channel Blockers; Rats; Rats, Inbred SHR; Tumor Cells, Cultured	1999

Article

Year

Different modes of action of the imidazoline compound RX871024 in pancreatic beta-cells. Blocking of K+ channels, mobilization of Ca2+ from endoplasmic reticulum, and interaction with exocytotic machinery.

Annals of the New York Academy of Sciences, 1999, Jun-21, Volume: 881

The imidazoline compound RX871024 glucose-dependently potentiates the release of insulin in pancreatic islets and beta-cell lines. This activity of the compound is not related to its action by stimulating alpha 2-adrenoceptors and I1- and I2-imidazoline receptors. There are at least three modes of action of RX871024 in beta-cells: (1) RX871024 blocks the ATP-dependent, Ca(2+)-activated, and delayed rectifier K+ channel activity; (2) RX871024 causes mobilization of Ca2+ from thapsigargin-sensitive intracellular stores, the effect probably controlled by cytochrome P450; and (3) the stimulatory activity of RX871024 on insulin release involves interaction of the compound with the exocytotic machinery, unrelated to the changes in membrane potential and cytoplasmic-free Ca2+ concentration, whereas protein phosphorylation plays an important role in this process. The maximal insulinotropic effect of RX871024 is much higher than that of the sulfonylurea glibenclamide. RX871024 stimulates insulin release and normalizes blood glucose levels in rats in vivo without affecting blood pressure and heart rate.

Topics: Animals; Blood Glucose; Blood Pressure; Calcium; Cells, Cultured; Cytoplasm; Endoplasmic Reticulum; Exocytosis; Heart Rate; Imidazoles; Indoles; Insulin; Insulin Secretion; Insulinoma; Islets of Langerhans; Kinetics; Male; Membrane Potentials; Models, Biological; Pancreatic Neoplasms; Phosphorylation; Potassium Channel Blockers; Rats; Rats, Inbred SHR; Tumor Cells, Cultured

1999