Am J Physiol Cell Physiol Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 282: C560-C566, 2002. First published October 31, 2001; doi:10.1152/ajpcell.00343.2001
0363-6143/02 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
282/3/C560    most recent
00343.2001v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (19)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Gupta, S.
Right arrow Articles by Keaney, J. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gupta, S.
Right arrow Articles by Keaney, J. F., Jr.
Vol. 282, Issue 3, C560-C566, March 2002

Hyperglycemia increases endothelial superoxide that impairs smooth muscle cell Na+-K+-ATPase activity

Sandeep Gupta1, Eugene Chough1, Jennifer Daley1, Peter Oates3, Keith Tornheim1, Neil B. Ruderman1, and John F. Keaney Jr.2

1 Diabetes and Metabolism Unit and 2 Whitaker Cardiovascular Institute, Evans Memorial Department of Medicine, Boston University School of Medicine, Boston, Massachusetts 02118; and 3 Division of Metabolic Research, Pfizer Central Research, Groton, Connecticut 06340

Nitric oxide (NO) plays an important role in the control of numerous vascular functions including basal Na+-K+-ATPase activity in arterial tissue. Hyperglycemia inhibits Na+-K+-ATPase activity in rabbit aorta, in part, through diminished bioactivity of NO. The precise mechanism(s) for such observations, however, are not yet clear. The purpose of this study was to examine the role of superoxide in modulating NO-mediated control of Na+-K+-ATPase in response to hyperglycemia. Rabbit aorta incubated with hyperglycemic glucose concentrations (44 mM) demonstrated a 50% reduction in Na+-K+-ATPase activity that was abrogated by superoxide dismutase. Hyperglycemia also produced a 50% increase in steady-state vascular superoxide measured by lucigenin-enhanced chemiluminescence that was closely associated with reduced Na+-K+-ATPase activity. Specifically, the hyperglycemia-induced increase in vascular superoxide was endothelium dependent, inhibited by L-arginine, and stimulated by Nomega -nitro-L-arginine. Aldose reductase inhibition with zopolrestat also inhibited the hyperglycemia-induced increase in vascular superoxide. In each manipulation of vascular superoxide, a reciprocal change in Na+-K+-ATPase activity was observed. Finally, a commercially available preparation of Na+-K+-ATPase was inhibited by pyrogallol, a superoxide generator. These data suggest that hyperglycemia induces an increase in endothelial superoxide that inhibits the stimulatory effect of NO on vascular Na+-K+-ATPase activity.

sodium-potassium adenosine 5'-triphosphatase; nitric oxide; endothelium; glucose


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
R. Ananthakrishnan, M. Kaneko, Y. C. Hwang, N. Quadri, T. Gomez, Q. Li, C. Caspersen, and R. Ramasamy
Aldose reductase mediates myocardial ischemia-reperfusion injury in part by opening mitochondrial permeability transition pore
Am J Physiol Heart Circ Physiol, February 1, 2009; 296(2): H333 - H341.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
E. Toth, A. Racz, J. Toth, P. M. Kaminski, M. S. Wolin, Z. Bagi, and A. Koller
Contribution of polyol pathway to arteriolar dysfunction in hyperglycemia. Role of oxidative stress, reduced NO, and enhanced PGH2/TXA2 mediation
Am J Physiol Heart Circ Physiol, November 1, 2007; 293(5): H3096 - H3104.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
W. Sun, P. J. Oates, J. B. Coutcher, C. Gerhardinger, and M. Lorenzi
A selective aldose reductase inhibitor of a new structural class prevents or reverses early retinal abnormalities in experimental diabetic retinopathy.
Diabetes, October 1, 2006; 55(10): 2757 - 2762.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
I. G. Obrosova, P. Pacher, C. Szabo, Z. Zsengeller, H. Hirooka, M. J. Stevens, and M. A. Yorek
Aldose Reductase Inhibition Counteracts Oxidative-Nitrosative Stress and Poly(ADP-Ribose) Polymerase Activation in Tissue Sites for Diabetes Complications
Diabetes, January 1, 2005; 54(1): 234 - 242.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
Z. Dagher, Y. S. Park, V. Asnaghi, T. Hoehn, C. Gerhardinger, and M. Lorenzi
Studies of Rat and Human Retinas Predict a Role for the Polyol Pathway in Human Diabetic Retinopathy
Diabetes, September 1, 2004; 53(9): 2404 - 2411.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
B.-L. Johansson, J. Wahren, and J. Pernow
C-peptide increases forearm blood flow in patients with type 1 diabetes via a nitric oxide-dependent mechanism
Am J Physiol Endocrinol Metab, October 1, 2003; 285(4): E864 - E870.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
I. G. Obrosova, A. G. Minchenko, R. Vasupuram, L. White, O. I. Abatan, A. K. Kumagai, R. N. Frank, and M. J. Stevens
Aldose Reductase Inhibitor Fidarestat Prevents Retinal Oxidative Stress and Vascular Endothelial Growth Factor Overexpression in Streptozotocin-Diabetic Rats
Diabetes, March 1, 2003; 52(3): 864 - 871.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online