Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1983;5:682-688

This Article
Right arrow Full Text (PDF)
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 PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lee, S. W.
Right arrow Articles by Wallick, E. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lee, S. W.
Right arrow Articles by Wallick, E. T.

Hypertension, Vol 5, 682-688, Copyright © 1983 by American Heart Association


ARTICLES

Decrease in Na+,K+-ATPase activity and [3H]ouabain binding sites in sarcolemma prepared from hearts of spontaneously hypertensive rats

SW Lee, A Schwartz, RJ Adams, Y Yamori, K Whitmer, LK Lane and ET Wallick

Na+,K+-ATPase activity, phosphorylation, and [3H]ouabain binding in sarcolemma isolated from spontaneously hypertensive rat (SHR) hearts were compared to the same parameters in sarcolemma from normotensive rat (WKY) hearts. Sarcolemma prepared from SHR heart contained significantly less ouabain-inhibitable ATPase activity than sarcolemma from WKY heart. No significant differences in sarcolemmal protein content or recovery were noted between the two groups. The numbers of phosphorylation sites and ouabain binding sites were lower for SHR hearts than for WKY hearts. The KD values for ouabain binding were the same (0.30 muM) in cardiac sarcolemma of SHR and WKY. The I50 values for inhibition by ouabain of Na+,K+-ATPase were also the same for both groups (SHR = 49 microM; WKY = 44 microM). These data suggest that the decrease of cardiac sarcolemmal Na+,K+-ATPase activity in SHR hearts is due to a decrease in the number of active sites.


This article has been cited by other articles:


Home page
Cardiovasc ResHome page
M. Galinanes and A. G Fowler
Role of clinical pathologies in myocardial injury following ischaemia and reperfusion
Cardiovasc Res, February 15, 2004; 61(3): 512 - 521.
[Abstract] [Full Text] [PDF]


Home page
EuropaceHome page
R. Wolk
Arrhythmogenic mechanisms in left ventricular hypertrophy
Europace, January 1, 2000; 2(3): 216 - 223.
[Abstract] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
J. L. Lundmark, R. Ramasamy, P. R. Vulliet, and S. Schaefer
Chelerythrine increases Na-K-ATPase activity and limits ischemic injury in isolated rat hearts
Am J Physiol Heart Circ Physiol, September 1, 1999; 277(3): H999 - H1006.
[Abstract] [Full Text] [PDF]


Home page
Cardiovasc ResHome page
R. Ramasamy, H. Liu, P. J Oates, and S. Schaefer
Attenuation of ischemia induced increases in sodium and calcium by the aldose reductase inhibitor Zopolrestat
Cardiovasc Res, April 1, 1999; 42(1): 130 - 139.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
C. Rodriguez-Sargent, E. S. Estape, N. Fernandez, J. E. Irizarry, J. L. Cangiano, and O. A. Candia
Altered Lens Short-Circuit Current in Adult Cataract-Prone Dahl Hypertensive Rats
Hypertension, September 1, 1996; 28(3): 440 - 443.
[Abstract] [Full Text]


Home page
Circ. Res.Home page
M. M. Pike, C. S. Luo, S. Yanagida, G. R. Hageman, and P. G. Anderson
23Na and 31P Nuclear Magnetic Resonance Studies of Ischemia-Induced Ventricular Fibrillation : Alterations of Intracellular Na+ and Cellular Energy
Circ. Res., August 1, 1995; 77(2): 394 - 406.
[Abstract] [Full Text]