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 ce ll 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 stimulato ry action of 100 nmol/l insulin on BMT-sensitive Na+/K+/2Cl(+)-cotrans porter was completely abolished by 10 mu mol/l lavendustin A (LAV-A, a n inhibitor of TK), however 100 nmol/l insulin could stimulate AML-sen sitive pathways even in LAV-A (10 mu mol/l)-treated cells. These obser vations indicate that the insulin (100 nmol/l) action on the BMT-sensi tive Na+/K+/2Cl(-) cotransporter is mediated through TK-dependent path ways, while 100 nmol/l insulin requires a TK-independent pathway to sh ow the stimulatory action on the AML-sensitive pathways. From these ob servations we conclude that TK-dependent and -independent pathways are involved in the insulin (100 nmol/l) signaling in fetal rat type II p neumocyte.