1.Functional roles of Na+/H+ exchanger isoforms in saliva secretion.
Keerang PARK ; Richard L EVANS ; James E MELVIN
Journal of Korean Medical Science 2000;15(Suppl):S5-S6
No abstract available.
Animal
;
Isomerism
;
Saliva/secretion*
;
Sodium-Hydrogen Antiporter/secretion
;
Sodium-Hydrogen Antiporter/physiology*
;
Sodium-Hydrogen Antiporter/chemistry*
2.Functional roles of Na+/H+ exchanger isoforms in saliva secretion.
Keerang PARK ; Richard L EVANS ; James E MELVIN
Journal of Korean Medical Science 2000;15(Suppl):S5-S6
No abstract available.
Animal
;
Isomerism
;
Saliva/secretion*
;
Sodium-Hydrogen Antiporter/secretion
;
Sodium-Hydrogen Antiporter/physiology*
;
Sodium-Hydrogen Antiporter/chemistry*
3.Intracellular acidosis decreases the outward Na(+)-Ca2+ exchange current in guinea pig ventricular myocytes.
Ek Ho LEE ; So Ra PARK ; Kwang Se PAIK ; Chang Kook SUH
Yonsei Medical Journal 1995;36(2):146-152
The Na(+)-Ca2+ exchange transport operating in outward mode has been suggested to cause Ca2+ entry during reperfusion or reoxygenation, exchanging extracellular Ca2+ for intracellular Na+ that has accumulated during ischemia or cardioplegia. During cardioplegia, however, an increase in Ca2+ entry via this mechanism can be decreased due to increased intracellular H+ activity and a decrease in cellular ATP content. In this study giant excised cardiac sarcolemmal membrane patch clamp technique was employed to investigate the effect of cytosolic pH change on the Na(+)-Ca2+ exchanger, excluding the effect of ATP, in guinea pig cardiac myocytes. The outward Na(+)-dependent current, which has a characteristics of Hill equation, was decreased as pH was decreased in the range of 7.5-6.5. The current density generated by the Na(+)-Ca2+ exchange transport was 56.6 +/- 4.4 pA/pF (Mean +/- S.E.M.) at pH 7.2 and decreased to 42.9 +/- 3.0 pA/pF at pH 6.9. These results imply that Na(+)-Ca2+ exchange transport, operating in a reverse mode during cardioplegia, decreases due to increased intracellular H+, and further suggest that consequent intracellular Na+ accumulation is one of aggravating factors for Ca2+ influx during reoxygenation or reperfusion.
Acidosis/*metabolism
;
Animal
;
Calcium/*metabolism
;
Electric Conductivity
;
Guinea Pigs
;
Heart Ventricle/metabolism
;
Hydrogen-Ion Concentration
;
Ion Transport
;
Myocardium/*metabolism
;
Sodium/*metabolism
;
Sodium-Hydrogen Antiporter/physiology
;
Support, Non-U.S. Gov't
4.A novel Na+-dependent transporter and NHE3 mediate H+ efflux in the luminal membrane of the pancreatic duct: regulation by cAMP.
Min Goo LEE ; Wooin AHN ; Joo Young CHOI ; Shmuel MUALLEM ; Kyung Hwan KIM
Journal of Korean Medical Science 2000;15(Suppl):S29-S30
No abstract available.
1-Methyl-3-isobutylxanthine/pharmacology
;
Ammonium Compounds/pharmacology
;
Animal
;
Biological Transport/physiology
;
Biological Transport/drug effects
;
Cell Membrane/metabolism
;
Cyclic AMP/metabolism*
;
Forskolin/pharmacology
;
Guanidines/pharmacology
;
Mice
;
Mice, Knockout
;
Pancreatic Ducts/metabolism*
;
Phosphodiesterase Inhibitors/pharmacology
;
Protons
;
Sodium-Hydrogen Antiporter/metabolism*
;
Sodium-Hydrogen Antiporter/genetics
;
Sulfones/pharmacology