Roles of tyrosine kinase in insulin action on cell volume of fetal rat type II pneumocyte

The aim of the present study was to investigate the roles of tyrosine kinase (TK) in the insulin action on cell volume in fetal rat (20-day gestational age) type II pneumocyte. Insulin (100 nmol/l) increased cell volume, and this insulin (100 nmol/l) action was completely blocked by 50 mu mol/l bumetanide (BMT) and 10 mu mol/l amiloride (AML). This observation indicates that 100 nmol/l insulin activates BMT-sensitive Na+/K+/2Cl(-) cotransporter and AML-sensitive pathways. The stimulatory action of 100 nmol/l insulin on BMT-sensitive Na+/K+/2Cl(+)-cotransporter was completely abolished by 10 mu mol/l lavendustin A (LAV-A, an inhibitor of TK), however 100 nmol/l insulin could stimulate AML-sensitive pathways even in LAV-A (10 mu mol/l)-treated cells. These observations indicate that the insulin (100 nmol/l) action on the BMT-sensitive Na+/K+/2Cl(-) cotransporter is mediated through TK-dependent pathways, while 100 nmol/l insulin requires a TK-independent pathway to show the stimulatory action on the AML-sensitive pathways. From these observations we conclude that TK-dependent and -independent pathways are involved in the insulin (100 nmol/l) signaling in fetal rat type II pneumocyte.