s-9871 and efaroxan

s-9871 has been researched along with efaroxan* in 2 studies

Reviews

1 review(s) available for s-9871 and efaroxan

ArticleYear
Characterization of the imidazoline binding site involved in regulation of insulin secretion.
    Annals of the New York Academy of Sciences, 1995, Jul-12, Volume: 763

    Topics: Agmatine; Animals; Benzofurans; Down-Regulation; Imidazoles; Imidazoline Receptors; Insulin; Insulin Secretion; Islets of Langerhans; Receptors, Drug

1995

Other Studies

1 other study(ies) available for s-9871 and efaroxan

ArticleYear
Antagonism of the stimulatory effects of efaroxan and glibenclamide in rat pancreatic islets by the imidazoline, RX801080.
    British journal of pharmacology, 1993, Volume: 110, Issue:3

    1. The imidazoline alpha 2-adrenoceptor antagonist, efaroxan, stimulates insulin secretion from rat isolated islets and antagonizes the ability of diazoxide to inhibit glucose-induced insulin secretion. These effects result from closure of ATP-sensitive potassium channels although the mechanisms involved have not been elucidated. 2. In the present work, we have examined the effects of a close structural analogue of efaroxan, RX801080, in rat isolated islets of Langerhans. RX801080 was found to be ineffective as a stimulator of insulin secretion and did not prevent the inhibition of insulin secretion mediated by diazoxide. 3. RX801080 acted as an antagonist of the actions of several imidazolines (efaroxan, phentolamine and midaglizole) in rat islets. It dose-dependently inhibited the ability of efaroxan to antagonize the effects of diazoxide in islets and also completely inhibited the direct stimulation of insulin secretion mediated by efaroxan. 4. RX801080 also antagonized the effects of the non-imidazoline, ATP-sensitive potassium channel blocker, glibenclamide, in rat islets. It inhibited both the capacity of glibenclamide to stimulate insulin secretion and the ability of glibenclamide to overcome the inhibitory effects of diazoxide in rat islets. 5. Antagonism of glibenclamide responses by RX801080 was not due to inhibition of binding of the sulphonylurea to its receptor on the pancreatic beta-cell. 6. The results suggest that imidazoline compounds and sulphonylureas interact with distinct binding sites on islet cells, but that these sites can interact functionally to control islet cell ATP-sensitive potassium channel activity and insulin secretion.

    Topics: Adrenergic alpha-Antagonists; Animals; Benzofurans; Binding, Competitive; Cell Membrane; Drug Interactions; Glyburide; Imidazoles; Imidazoline Receptors; Insulin; Insulin Secretion; Islets of Langerhans; Kinetics; Male; Rats; Rats, Wistar; Receptors, Drug; Stimulation, Chemical

1993