ACELL September 46/3
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چکیده
Light, Douglas B., Tracy L. Capes, Rachel T. Gronau, and Matthew R. Adler. Extracellular ATP stimulates volume decrease in Necturus red blood cells. Am. J. Physiol. 277 (Cell Physiol. 46): C480–C491, 1999.—This study examined whether extracellular ATP stimulates regulatory volume decrease (RVD) in Necturus maculosus (mudpuppy) red blood cells (RBCs). The hemolytic index (a measure of osmotic fragility) decreased with extracellular ATP (50 μM). In contrast, the ATP scavenger hexokinase (2.5 U/ml, 1 mM glucose) increased osmotic fragility. In addition, the ATP-dependent K1 channel antagonist glibenclamide (100 μM) increased the hemolytic index, and this inhibition was reversed with ATP (50 μM). We also measured cell volume recovery in response to hypotonic shock electronically with a Coulter counter. Extracellular ATP (50 μM) enhanced cell volume decrease in a hypotonic (0.53) Ringer solution. In contrast, hexokinase (2.5 U/ml) and apyrase (an ATP diphosphohydrolase, 2.5 U/ml) inhibited cell volume recovery. The inhibitory effect of hexokinase was reversed with the Ca21 ionophore A-23187 (1 μM); it also was reversed with the cationophore gramicidin (5 μM in a choline-Ringer solution), indicating that ATP was linked to K1 efflux. In addition, glibenclamide (100 μM) and gadolinium (10 μM) inhibited cell volume decrease, and the effect of these agents was reversed with ATP (50 μM) and A-23187 (1 μM). Using the whole cell patch-clamp technique, we found that ATP (50 μM) stimulated a whole cell current under isosmotic conditions. In addition, apyrase (2.5 U/ml), glibenclamide (100 μM), and gadolinium (10 μM) inhibited whole cell currents that were activated during hypotonic swelling. The inhibitory effect of apyrase was reversed with the nonhydrolyzable analog adenosine 58-O-(3-thiotriphosphate) (50 μM), and the effect of glibenclamide or gadolinium was reversed with ATP (50 μM). Finally, anionic whole cell currents were activated with hypotonic swelling when ATP was the only significant charge carrier, suggesting that increases in cell volume led to ATP efflux through a conductive pathway. Taken together, these results indicate that extracellular ATP stimulated cell volume decrease via a Ca21-dependent step that led to K1 efflux.
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ACELL September 46/3
Dodd, J. S., J. A. Raleigh, and T. S. Gross. Osteocyte hypoxia: a novel mechanotransduction pathway. Am. J. Physiol. 277 (Cell Physiol. 46): C598–C602, 1999.—Bone is a unique tissue in which to examine mechanotransduction due to its essential role in weight bearing. Within bone, the osteocyte is an ideal cellular mechanotransducer candidate. Because osteocytes reside distant from the blood supp...
متن کاملACELL September 46/3
Zeiske, Wolfgang, Ilse Smets, Marcel Ameloot, Paul Steels, and Willy Van Driessche. Intracellular pH shifts in cultured kidney (A6) cells: effects on apical Na1 transport. Am. J. Physiol. 277 (Cell Physiol. 46): C469–C479, 1999.—We report, for the epithelial Na1 channel (ENaC) in A6 cells, the modulation by cell pH (pHc) of the transepithelial Na1 current (INa), the current through the individu...
متن کاملACELL September 46/3
Shepard, Allan R., and James L. Rae. Electrically silent potassium channel subunits from human lens epithelium. Am. J. Physiol. 277 (Cell Physiol. 46): C412–C424, 1999.—We describe the cloning and characterization of the first human members, hKv9.1 and hKv9.3, of the electrically silent delayed-rectifying-like K1 channel subfamily. Their modulatory effects on the electrically active subfamily m...
متن کاملACELL September 46/3
Stevens, Randel J., Jeffery S. Weinert, and Nelson G. Publicover. Visualization of origins and propagation of excitation in canine gastric smooth muscle. Am. J. Physiol. 277 (Cell Physiol. 46): C448–C460, 1999.—The origin and spread of excitation were visualized with fluo 3 fluorescence in tissues isolated from canine gastric antrum. Sheets of circular muscle (5 3 6 mm) had at least 1 (30%) and...
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JOHN M. PARK,1 ROSALYN M. ADAM,1 CRAIG A. PETERS,1 PAUL D. GUTHRIE,1 ZIJIE SUN,2 MICHAEL KLAGSBRUN,3 AND MICHAEL R. FREEMAN3 1Urologic Laboratory, Department of Urology, 3Laboratory for Surgical Research, Children’s Hospital, and Department of Surgery, Harvard Medical School, Boston, Massachusetts 02115; and 2Departments of Surgery and Genetics, Stanford University School of Medicine, Stanford,...
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