Couturier E, Malaisse W J
Diabetologia. 1980 Oct;19(4):335-40. doi: 10.1007/BF00280516.
Hypoglycaemic sulphonamides stimulate net uptake of 45Ca++ and insulin release in isolated pancreatic islets. These effects are antagonized by organic calcium-antagonists (e.g. suloctidil). In an artificial system, hypoglycaemic sulphonamides, such as gliclazide, stimulate the translocation of calcium into or across a hydrophobic immiscible domain, a process enhanced by the antibiotic ionophore A 23187 and antagonized by suloctidil. In this artificial system, the A 23187-mediated process of calcium countertransport is stimulated by gliclazide and inhibited by diazoxide. It is postulated that the insulinotropic action of hypoglycaemic and hyperglycaemic sulphonamides is primarily attributable to the ionophoretic action of these drugs.
降血糖磺酰胺类药物可刺激离体胰岛对45Ca++的净摄取及胰岛素释放。这些效应可被有机钙拮抗剂（如舒洛地尔）所拮抗。在一个人工系统中，降血糖磺酰胺类药物，如格列齐特，可刺激钙转运进入或穿过一个疏水不混溶区域，抗生素离子载体A 23187可增强这一过程，而舒洛地尔则可拮抗该过程。在这个人工系统中，格列齐特可刺激A 23187介导的钙反向转运过程，而二氮嗪则可抑制该过程。据推测，降血糖和升血糖磺酰胺类药物的促胰岛素作用主要归因于这些药物的离子载体作用。
