title: Activation of a Cl-dependent K flux by cAMP in pig red cells.
abstract: Activation of a Cl-dependent K flux by adenosine 3',5'-cyclic monophosphate (cAMP) was characterized in pig red cells, a cell type that lacks both the Ca-activated K channel and the Na-K-Cl cotransport pathway. As in other red cells, both Cl-dependent K efflux and K influx are stimulated on cell swelling. Although pig red cells fail to respond to beta-adrenergic stimuli, it is possible to raise the intracellular cAMP content by preincubating cells in the presence of 1 mM cAMP. The Cl-dependent K flux was compared in cells having a basal cAMP content of approximately 0.29 nmol/g hemoglobin vs. cAMP-loaded cells having approximately 8.4 nmol cAMP/g hemoglobin. Loading with cAMP stimulated both Cl-dependent K efflux and influx of hypotonically swollen cells. In maximally swollen cells whose volume was increased by approximately 17%, the Cl-dependent Rb influx occurs with a maximum velocity (Vmax) of 17.9 +/- 3.2 mumol.g hemoglobin (Hb)-1.h-1 and Km for Rb of 22.9 +/- 4.1 mM. In cAMP-loaded cells, both Vmax and Km were increased to 59.8 +/- 8.5 mumol.g Hb-1.h-1 and 63.1 +/- 8.8 mM, respectively. The Cl-dependent Rb influx is much larger in young cells than in old cells. However, both cell types respond to cAMP activation. Whereas cAMP and its analogues, 8-bromoadenosine 3',5'-cyclic monophosphate and dibutyryl adenosine 3',5'-cyclic monophosphate are stimulatory, AMP and guanosine 3',5'-cyclic monophosphate (cGMP) are not. These findings suggest that, like other ion transport systems, the Cl-dependent K flux of pig red cells is endowed with the capacity to respond to cAMP.
authors.affiliation: Department of Pharmacology, School of Medicine, University of Missouri-Columbia 65212.
authors.forename: H D
authors.initials: HD
authors.lastname: Kim
authors.forename: S
authors.initials: S
authors.lastname: Sergeant
authors.forename: L R
authors.initials: LR
authors.lastname: Forte
authors.forename: D H
authors.initials: DH
authors.lastname: Sohn
authors.forename: J H
authors.initials: JH
authors.lastname: Im
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D015124:8-Bromo Cyclic Adenosine Monophosphate / Q000494:pharmacology; D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D003994:Bucladesine / Q000494:pharmacology; D002034:Bumetanide / Q000494:pharmacology; D002118:Calcium / Q000097:blood; D002352:Carrier Proteins / Q000097:blood; D002712:Chlorides / Q000494:pharmacology*; D000242:Cyclic AMP / Q000097:blood / Q000494:pharmacology*; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D005033:Ethylmaleimide / Q000494:pharmacology; D005665:Furosemide / Q000494:pharmacology; D007700:Kinetics; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000097:blood*; D012413:Rubidium / Q000097:blood; D028021:Sodium-Potassium-Chloride Symporters; D013552:Swine; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D002352:Carrier Proteins; D002712:Chlorides; D028021:Sodium-Potassium-Chloride Symporters; D002034:Bumetanide; D015124:8-Bromo Cyclic Adenosine Monophosphate; D012856:4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid; D010042:Ouabain; D003994:Bucladesine; D005665:Furosemide; D000242:Cyclic AMP; D012413:Rubidium; D013755:Tetradecanoylphorbol Acetate; D005033:Ethylmaleimide; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid; D011188:Potassium; D002118:Calcium