[Effects of inhibitors of intracellular signal transduction on lipopolysaccharide-induced increase in permeability of cultured pulmonary endothelial cell monolayers].

To investigate the mechanism of lipopolysaccharide (LPS)-induced endothelial response, we measured the permeability to albumin of cultured pulmonary endothelial cell monolayers. PMA and SC-9, used as activators for protein kinase C (PCK), failed to cause an increase in permeability to albumin. H-7, a potent PKC inhibitor, did not prevent the LPS-induced increase in permeability to albumin. In contrast, H-8, which strongly inhibits cyclic nucleotide-dependent protein kinases, and a calmodulin antagonist prevented the LPS-induced increase in permeability to albumin. These results suggest that calmodulin and protein kinases other than PCK are implicated in the mechanism of LPS-induced increase in permeability to albumin.