What are the mechanism of action of sulfonylureas?

These drugs exert their hypoglycaemic effects by stimulating insulin secretion from the pancreatic beta-cell. Their primary mechanism of action is to close ATP-sensitive K-channels in the beta-cell plasma membrane, and so initiate a chain of events which results in insulin release.

What is the mechanism of action of glimepiride?

Mechanism of action Like all sulfonylureas, glimepiride acts as an insulin secretagogue. It lowers blood sugar by stimulating the release of insulin by pancreatic beta cells and by inducing increased activity of intracellular insulin receptors.

Which second generation sulfonylureas have additional antiplatelet action?

Gliclazide is a second generation, sulfonylurea oral hypoglycemic agent, with a pharmacology broadly similar to that of tolbutamide but a potency similar to that of glyburide, and is used in the treatment of type 2 diabetes. It may also have blood glucose independently antiplatelet properties.

What is the mechanism of action of sulfonylureas?

Their primary mechanism of action is to close ATP-sensitive K-channels in the beta-cell plasma membrane, and so initiate a chain of events which results in insulin release.

How does sulfonylureas work on the pancreatic beta cell?

These drugs exert their hypoglycaemic effects by stimulating insulin secretion from the pancreatic beta-cell. Their primary mechanism of action is to close ATP-sensitive K-channels in the beta-cell plasma membrane, and so initiate a chain of events which results in insulin release.

How are sulfonylureas used to treat diabetes mellitus?

Sulfonylureas are widely used to treat non-insulin dependent diabetes mellitus. These drugs exert their hypoglycaemic effects by stimulating insulin secretion from the pancreatic beta-cell. Their primary mechanism of action is to close ATP-sensitive K-channels in the beta-cell plasma membrane, and so initiate a chain of events which results in

How does sulfonylurea bind to the potassium channel?

They primarily act by binding to the SUR subunit of the ATP-sensitive potassium (K ATP) channel and inducing channel closure. However, the channel is still able to open to a limited extent when the drug is bound, so that high-affinity sulfonylurea inhibition is not complete, even at saturating drug concentrations.