cAMP activates Na+/H+ antiporter in murine macrophages.
The role of cAMP in activating the Na+/H+ antiporter in murine macrophage (M phi) system was investigated. Incubation of PU5-1.8 macrophage tumour cells, peritoneal M phi and bone marrow derived macrophages (BMDM phi s) with dibutyryl-cAMP (db-cAMP) or cholera toxin (CT) led to an increase in intracellular pH (pHi). The magnitudes of these responses differed markedly in the three cell types, BMDM phi s being the most sensitive, PU5-1.8 cells the least so. These cells also differed in their responses to inhibitors of Na+/H+ exchange. In PU5-1.8 cells, the db-cAMP- or CT-triggered intracellular alkalinization was abolished by amiloride treatment which, however, was ineffective in BMDM phi s. The chemotactic peptide, N-formyl-methionyl-leucyl-phenylalanine (FMLP), also caused a significant increase in cytoplasmic pH. However, its action was apparently not mediated by cAMP. The significance of these observations is discussed.
Kong
S K
SK
Department of Biochemistry, Chinese University of Hong Kong, Shatin, NT.
Choy
Y M
YM
Fung
K P
KP
Lee
C Y
CY
D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology*; D002352:Carrier Proteins / Q000378:metabolism*; D002460:Cell Line; D002772:Cholera Toxin / Q000494:pharmacology; D000242:Cyclic AMP / Q000502:physiology*; D006412:Hematopoietic Stem Cells / Q000166:cytology; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D008264:Macrophages / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D009240:N-Formylmethionine Leucyl-Phenylalanine / Q000494:pharmacology; D017923:Sodium-Hydrogen Exchangers
D002352:Carrier Proteins; D017923:Sodium-Hydrogen Exchangers; D009240:N-Formylmethionine Leucyl-Phenylalanine; D003994:Bucladesine; D000584:Amiloride; D002772:Cholera Toxin; D000242:Cyclic AMP